Pubmed abstracts for Protein-Protein Interaction search result :

Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.75355037
Upon loss of the MCL 1 BAK complex , BAK complexed with either BAX in proapoptotic E1B mutant adenovirus infected cells , or with the adenovirus BCL 2 homolog E1B 19K in cells infected with the wild type virus in which apoptosis is inhibited . 0.75355037^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.58895376
Surprisingly , zebrafish Bax 2 ( zBax 2 ) was homologous to mammalian Bax by sequence and synteny , yet demonstrated functional conservation with human Bak . 0.58895376^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition to Bax , Gfi 1 also represses Bak , another apoptosis promoting member of the Bcl 2 gene family . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
By contrast , levels of Bcl 2 , and two other Bcl 2 family members , Bax and Bak , remained unaltered . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Of the bcl 2 family members , IFN gamma directly induced bak but notably not bax , which is activated by p 53 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The Bcl 2 family members analyzed were Bcl 2 , Bcl 10 , Bax , Bad , Bak , A 1 , and Mcl 1 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The cellular bax and bak genes , which are known to accelerate cell death , also accelerate virus induced apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
None of the cytokines tested caused a change in the levels of expression of Bcl 2 , Bax , Bcl 10 , or Bak proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 , Mcl 1 , and also Bax and Bak , but not p 53 were demonstrable in the tumor cells by immunostaining . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , the proapoptotic proteins , bax and bak seemed to be constitutively expressed . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
After Ad5CMVE2F 1 infection , expression of Bax and Bak was unchanged , whereas Mcl 1 levels decreased markedly . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
HCl treatment up regulated Bax and Bak expression , down regulated Bcl 2 expression , and activated caspase 3 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 , Bcl xL , Bad , Bak , and Bax levels were not altered by either treatment . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Certain BCL 2 family proapoptotic proteins such as BAX and BAK share extensive sequence homology with BCL 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The levels of proapoptotic proteins Bax , BAD , and Bak were not significantly altered . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
With hypergastrinemia , the expression of Bcl 2 and Bak was increased and Bax decreased in the middle of the gland . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Other members of the Bcl 2 family ( Bag 1 , Bak , Bax , and Bcl xL ) were not altered in expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax delta ( 16 kDa ) was highly represented in normal keratinocytes , and levels of bak were variable between cell lines . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
None of the hormone treatments altered the proapoptotic protein levels , bax and bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
During tumour regression , clusterin and Bax proteins were elevated but Bak , Bcl xl and Bcl 2 were unchanged . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The apoptosis cascade up regulated Bax and Bak protein , down regulated Bcl xL protein , and activated caspase 3 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Apoptosis : Bax to Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of other members of the Bcl 2 family such as Bax , Bcl 10 ( L ) and Bak were not affected . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cytochrome C release seemed to be triggered by transcriptional activation of Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Further , murine embryonic fibroblasts from bax ( / ) bak ( / ) mice did not die in response to oxygen deprivation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The initiation of apoptosis by DNA damage signals was shown to absolutely depend on the expression of either Bax or Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of Bax , Bcl 2 , Bak , and Bcl 10 ( L ) was analyzed by immunoblotting . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In the I / R group , up regulation of Bax , Bak , and caspase 3 was observed . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The proteins studied were Bcl 2 , Bcl xL ( anti apoptotic ) , Bax , Bad , Bak , and Bcl xS ( pro apoptotic ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak : back bone of T cell death . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
No significant variations in the levels of Bcl 2 , Bax and Bak proteins were noticed upon treatment with 2CdA . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
However , loss of Bax , Bak and Bcl Xs did not compromise sensitivity to TRAIL . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Western blot analysis was performed with anti ERK1 / 2 , Mcl 1 , Bak , Bcl 10 and Bax antibodies . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The proapoptotic proteins Bax and Bak are not involved in Wallerian degeneration . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
However , the expression levels of Bcl 2 , Bax , Bak , and Mcl 1 were unchanged . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The multidomain proapoptotic molecules BAK or BAX are required to initiate the mitochondrial pathway of apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Impact of proapoptotic proteins Bax and Bak in tumor progression and response to treatment . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Extra mitochondrial HSP 60 complexes with both bax and bak , but not with bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 , Bax , Bak , Bid , and A 1 were used as indicators for activation of the mitochondrial pathway . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak ) at the mitochondrial surface . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
CAPE application also enhanced the expression of p 53 , Bax , and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The induction of apoptosis depends on Bax and Bak , two proapoptotic proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The steady state mRNA levels of Bax , Bad and Bak were not significantly changed for 48 h of C 2 ceramide treatment . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Other proapoptotic proteins ( e . g . , BAX , BAK , BIM ) promote release of cytochrome C . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Fatal liaisons of p 53 with Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , it induced up regulation of the Bcl 2 family proapoptotic proteins , Bim , Bax , and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 10 ( L , ) Bax , and Bak were expressed at similar levels in cardiac , dermal , and lung fibroblasts . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Gene expresssion of the pro apoptotic genes BAK and BAX was lowered compared to expression in ' normal ' myocardium . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , Bcl 2 , Bcl xL , Bax , and Bak localized in the mitochondria were detected . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
RT PCR was used to measure changes in Bcl 2 , Bax , Bad , Bak , P 53 , ICE and Fas . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
T 3 treatment resulted in increase in mitochondrial Bax and Bak together with decreased mitochondrial Bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In the heart , this cytosolic HSP 60 complexes with Bax , Bak and Bcl XL , but not with Bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
When the gene encoding F1L was deleted from MVA , apoptosis resulted that required Bak or Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Furthermore , fibroblast cells deficient in Bax and Bak , but not Bid , were resistant to bleomycin induced cell death . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
E1B 19K is a BCL 2 homolog that binds and inactivates proapoptotic BAK and BAX . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Mouse embryonic fibroblasts deficient for Bax and / or Bak were protected from Legionella induced caspase activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cell death in the absence of Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Depending on cell type and apoptotic inducer , Bax and / or Bak are structural component ( s ) of MAC . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Justicidin A also reduced Bcl 10 ( L ) and increased Bax and Bak in mitochondria . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Regulated targeting of Bax and Bak to intracellular membranes during apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In mammals , the multidomain proteins ( MDPs ) of the Bcl 2 family include Bax , Bak , and Bok . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In transient transfection assays , Bik promotes cell death in a manner similar to the death promoting members of the Bcl 2 family , Bax and Bak . ^^^ While Bik does not show overt homology to the BH 1 and BH 2 conserved domains characteristic of the Bcl 2 family , it does share a 9 amino acid domain ( BH 3 ) with Bax and Bak which may be a critical determinant for the death promoting activity of these proteins . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Like Bax , the bak gene product primarily enhances apoptotic cell death following an appropriate stimulus . ^^^ Unlike Bax , however , Bak can inhibit cell death in an Epstein Barr virus transformed cell line . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Specific mutations that disrupt the ability of Bcl XL to interact with Bax or Bak still preserve 70 80 % of the anti death activity of wild type Bcl XL . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Taken together , these results suggest that expression of Bcl XL is increased in undifferentiated primary colorectal cancers , often with accompanying reciprocal decreases in the anti apoptotic proteins Bcl 2 and Mcl 1 and the pro apoptotic protein Bak , whereas Bax expression is relatively constant . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This protective effect of Bcl 2 occurs in the absence of significant variations , in the stimulated livers , in the level of expression of other proteins also involved in resistance or sensitivity to apoptosis , namely Bcl 10 , Bax , Bad , Bak , and p 53 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Thus , like Bcl 2 and Bcl 10 , the Bcl w protein promotes cell survival , in contrast to other close homologues , Bax and Bak , which facilitate cell death . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak are Bcl 2 family members which contain Bcl 2 homology regions 1 , 2 , and 3 ( BH 1 , BH 2 , and BH 3 ) , which interact with E1B 19K and Bcl 2 and promote apoptosis . ^^^ Like Bax and Bak , Nbk was cloned from a yeast two hybrid screen for proteins that interact with E1B 19K . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The apoptosis regulating proteins Bcl 2 , Bax , Bcl 10 , Bak , and Mcl 1 were examined by immunohistochemical methods in 48 archival specimens of adenocarcinoma of the stomach , and the results were correlated with tumor histology ( intestinal versus diffuse pattern ) and clinical stage ( early versus late stage disease , ie , stages 1 and 2 versus stage 3 ) . ^^^ Tumor cells containing immunostaining for the anti apoptotic proteins Bcl 2 , Bcl 10 , and Mcl 1 were present in 26 ( 54 % ) , 41 ( 85 % ) , and 36 ( 75 % ) of the 48 cases evaluated , respectively , whereas immunopositivity for the pro apoptotic proteins Bax and Bak was found in 44 ( 92 % ) and 42 ( 88 % ) specimens Comparisons of these immunostaining results with tumor histology revealed statistically significant differences for Bax ( P = 0 . 03 ) , Bcl 10 ( P = 0 . 003 ) , and Mcl 1 ( P = 0 . 005 ) , which were all more frequently immunopositive for tumors with an intestinal than a diffuse histological pattern ( chi 2 analysis ) . ^^^ In contrast , the percentage of Bcl 2 immunopositive tumor cells was higher in tumors with diffuse histology compared with intestinal ( 32 + / 5 % versus 12 + / 5 % ; P = 0 . 01 ) , whereas the percentages of Bax and Bak immunopositive tumor cells were not significantly different between these two histological types . ^^^ The immunointensity for the Bcl 2 , Bcl 10 , and Mcl 1 proteins was stronger in tumor cells compared with normal foveolar cells in 7 ( 21 % ) , 15 ( 44 % ) , and 8 ( 2 . 1 % ) of 34 cases , respectively , whereas the immunointensity of the proapoptotic proteins Bax and Bak was reduced compared with normal cells in 8 ( 24 % ) and 24 ( 71 % ) cases . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Since the discovery of Bcl 2 a decade ago , several other cellular and viral genes encoding homologous proteins have been identified , some of which suppress cell death akin to Bcl 2 ( Bcl XL , Mcl 1 , A1 / Bfl 1 , Nr 13 , Ced 9 , BHRF 1 ) and others which promote apoptosis ( Bax , Bcl Xs , Bak , Bik , Bad ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Apoptosis resistance in the metastatic cells was associated with higher levels of expression of the cell death suppressor BCL 2 and lower levels of the death promoters BAX and BAK than were detected in the nonmetastatic LNCaP Pro 5 cells , whereas levels of two other BCL 2 family members ( BCL 10 ( L ) and BAD ) were indistinguishable . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The pro apoptotic protein bax was expressed at lower levels in carcinomas than in adenomas , whereas bak and bclx were expressed in the same order of magnitude in all tissues examined . ^^^ In all four cell lines , the amounts of the pro apoptotic proteins bax , bak and bclx were higher than in most tumor tissues . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A Bcl 2 homolog encoded by Kaposi sarcoma associated virus , human herpesvirus 8 , inhibits apoptosis but does not heterodimerize with Bax or Bak . ^^^ Interestingly , KS bcl 2 neither homodimerizes nor heterodimerizes with other Bcl 2 family members , suggesting that KSbcl 2 may have evolved to escape any negative regulatory effects of the cellular Bax and Bak proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Biochemical analysis revealed that all three proteins can associate with Bax and Bak , members of the Bcl 2 protein subfamily that can facilitate apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The BH 1 and BH 2 homology domains are highly conserved in ORF 16 , and ORF 16 heterodimerizes with Bcl 2 family members Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
However , using quantitative plate binding assays , we now show that Bax as well as peptides derived from the BH 3 domains of Bax and Bak block both Bcl 2 / Bax binding and Bcl 2 / Bcl 2 binding . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The product of harakiri , Hrk , physically interacts with the death repressor proteins Bcl 2 and Bcl 10 ( L ) , but not with death promoting homologs , Bax or Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The three pro apoptotic members of the family , Bak , Bad , and Bax , all showed an early decline in mRNA levels when Bcl 10 transcripts increased , followed by later peaks at 12 , 24 , and 48 to 72 hours , respectively . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Only Bax and Bak killed yeast via a process that did not require interleukin 1beta converting enzyme like proteases . ^^^ Bax / Bak lethality was suppressed by coexpression of Bcl 2 family members that are anti apoptotic in vertebrates , namely Bcl xL , Bcl 2 , Mcl 1 , and A 1 . ^^^ These inactive proteins bound to anti apoptotic members of the Bcl 2 family but not to Bax or Bak . ^^^ In contrast , most Bcl 2 family proteins that attenuated death bound to Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Preablation biopsy specimens and prostatectomy specimens were immunohistochemically stained for apoptotic cells and for expression of apoptosis regulatory proteins Bcl 2 , Bax , Bcl 10 , and Bak . ^^^ In all 26 specimens , benign prostatic hyperplasia demonstrated increased expression of the Bcl 2 protein , but no change in the expression of Bax , Bcl 10 , and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak induced cell death in the fission yeast Schizosaccharomyces pombe . ^^^ The effects of the expression of the human Bcl 2 family proteins Bax , Bak , Bcl 2 , and Bcl XL were examined in the fission yeast Schizosaccharomyces pombe and compared with Bax induced cell death in mammalian cells . ^^^ Expression of the proapoptotic proteins Bax and Bak conferred a lethal phenotype in this yeast , which was strongly suppressed by coexpression of the anti apoptotic protein Bcl XL . ^^^ However , other features distinguished Bax and Bak induced death in S . pombe from animal cell apoptosis . ^^^ Electron microscopic analysis of S . pombe cells dying in response to Bax or Bak expression demonstrated massive cytosolic vacuolization and multifocal nuclear chromatin condensation , thus distinguishing this form of cell death from the classical morphological features of apoptosis seen in animal cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Analysis of bi transgenic K rasVal 12 10 TAgWt mice homozygous for wild type or null p 53 alleles established that the enhancement of apoptosis occurs through a p 53 independent mechanism , is not attributable to augmented proliferation or to an increase in abortive cell cycle reentry ( compared to TAgWt mice ) , and is not associated with detectable changes in the crypt villus patterns of expression of apoptotic regulators ( Bcl 2 , Bcl xL , Bak , and Bax ) or mediators of epithelial cell matrix interactions and survival ( e . g . , alpha5beta1 integrin and its ligand , fibronectin ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of the BCL 2 protein family members , BAX , BAK , BAD , BCL xL , BCL xS , and BCL 2 , was measured ( by western blotting using specific antibodies ) in PC 12 cells before and during apoptosis induced by either H2O2 treatment or by serum deprivation and during rescue from apoptosis by nerve growth factor ( NGF ) . ^^^ H2O2 induced apoptosis , as measured by DNA fragmentation , caused : ( a ) a dose dependent increase in BAX , ( b ) a dose independent increase in BAK , and ( c ) a dose dependent inhibition of BAD expression . ^^^ By comparison , apoptosis induced by serum deprivation resulted in a time dependent decrease in both BAX and BAK , along with a dramatic and sudden decrease in BAD expression . ^^^ However , when PC 12 cells were incubated in an apoptosis sparing medium ( i . e . , NGF supplemented serum free medium ) , both BAX and BAK were increased significantly , whereas BAD expression remained inhibited . ^^^ Our results show that the expression of BAX , BAK , BAD , and BCL xL is altered in a stimulus dependent manner but can not be used to define whether a cell will undergo or survive apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Remarkably , reentry of villus enterocytes to the cell cycle increases the radiosensitivity of the crypt epithelium without changing Bcl 2 , Bcl xL , Bak , or Bax expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Other proteins , like bcl xL , A 1 or mcl 1 have the same anti apoptotic function , but several molecules of the same family , like bcl xS , bax alpha or bak can trigger the opposite effect . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Mutation of a tyrosine residue within the conserved N terminal BH 4 region had no effect on the ability of Bcl 2 or its closest homologs to enhance cell survival and did not prevent heterodimerization with death enhancing family members Bax , Bak , Bad and Bik . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
It shares a conserved domain , BH 3 , with other pro apoptotic proteins , Bax , Bak , Bid , and Hrk , and certain anti apoptosis proteins such as Bcl 2 and Bcl xL . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Three human colonic adenoma cell lines ( AA / C1 , RG / C2 and BH / C1 ) and one carcinoma cell line ( S / KS / FI ) were used to determine the effects of butyrate on the expression of bcl 2 , bax and bak to examine the possible role of these proteins in the induction of apoptosis . ^^^ RG / C2 and BH / C1 cells express p 26 bcl 2 and butyrate treatment decreased p 26 bcl 2 levels in association with apoptosis , whereas bax and bak levels remained constant . ^^^ In S / KS / FI cells , bax or bak levels did not change in response to butyrate . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Protein expression of Fas / APO 1 or bcl 2 , and messenger RNA ( mRNA ) expression of bcl 2 , bcl xL , bax , bak , Fas / APO 1 , Fas ligand ( Fas L ) , c myc , mad , or max were determined . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of several other bcl 2 family members ( bcl 10 , ich 1 , bax , bag , and bak ) and retinoid receptors ( RARalpha , RXRalpha , and RXRbeta ) was not affected by treatment with RAR and / or RXR activating retinoids ; RARbeta RNA was undetectable before and after retinoid treatment . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This finding is in direct contrast to the ability of other pro apoptotic members ( Bax , Bak , and Bik ) to interact with all of the anti apoptotic proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A 26 amino acid peptide within this domain , which showed significant homology to the alpha helical BH 3 domains of related apoptotic proteins like Bak and Bax , was found to be necessary and sufficient to bind Bcl xL . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Consequently , the E1B 19K and Bcl 2 proteins bind to and inhibit the cellular death inducing proteins Bax , Bak and Nbk / Bik . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
BH 3 domains from the pro apoptotic proteins Bax and Bak , but not the BH 3 domain of the anti apoptotic protein Bcl 2 , induced apoptosis in this system , as determined by the rapid activation of specific apoptotic proteases ( caspases ) and by DNA fragmentation . ^^^ These results support a model in which pro apoptotic proteins , such as Bax and Bak , bind to Bcl 2 via their BH 3 domains , inactivating the normal ability of Bcl 2 to suppress apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Thus , as previously shown for BAX , BAK , BCL 2 , and BCL XL , the BH 3 domain of BAD is required for its dimerization with other BCL 2 family proteins . ^^^ BAD was further analyzed for its ability to bind to various mutants of BCL 2 and BCL XL that have lost the ability to bind BAX and BAK , some of which retain biological activity and some of which do not . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The pattern of endogenous expression levels of Bax , Bcl 2 , Bcl 10 and Bak , which was not modulated by cisplatin treatment , demonstrated that these Bcl 2 family proteins are not involved in drug induced apoptosis in the TGCT cell lines . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Deletion of BH 4 rendered Bcl 2 ( and Bcl xL ) inactive but did not impair either Bcl 2 homodimerization or ability to bind to Bax or five other pro apoptotic relatives ( Bak , Bad , Bik , Bid or Bim ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Apoptosis and cell proliferation were determined by immunocytological techniques and the markers p 53 , p21WAF / Cip , Bax , Bak , Bcl 2 , cyclin D 1 and PCNA , and also screened for signal transduction indicators such as c H ras , c fos and raf 1 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , the pro apoptotic proteins Bax and Bak were detected in all 11 cell lines , and were present at relatively higher levels in 10 and 5 of the 11 lines , respectively . ^^^ Immunoblot analysis of primary adenocarcinomas revealed expression of the anti apoptotic proteins Bcl 2 , Bcl 10 ( L ) , Mcl 1 , and BAG 1 , as well as the pro apoptotic proteins Bax , Bak , and CPP 32 , in at least 2 of the 3 tumors examined . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Alteration of proteins regulating apoptosis , Bcl 2 , Bcl 10 , Bax , Bak , Bad , ICH 1 and CPP 32 , in Alzheimer ' s disease . ^^^ Apoptosis is regulated by the B cell leukemia 2 gene product ( Bcl 2 ) family ( Bcl 2 , Bcl 10 , Bax , Bak and Bad ) and the caspase family ( ICH 1 and CPP 32 ) , with apoptosis being prevented by Bcl 2 and Bcl 10 , and promoted by Bax , Bak , Bad , ICH 1 and CPP 32 . ^^^ In the cytosolic fractions , the level of Bcl 10 beta was increased , while Bcl xL , Bax , Bak , and Bad and ICH 1L were unchanged . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of several apoptosis regulating proteins , including the Bcl 2 family proteins Bcl 2 , Bcl XL , Mcl 1 , Bax , Bak , and BAD ; the Bcl 2 binding protein BAG 1 ; and the cell death protease Caspase 3 ( CPP 32 ) , was evaluated by immunoblotting using 58 peripheral blood B CLL specimens from previously untreated patients . ^^^ Expression of Bcl 2 , Mcl 1 , BAG 1 , Bax , Bak , and Caspase 3 was commonly found in circulating B CLL cells , whereas the Bcl XL and BAD proteins were not present . ^^^ Apoptosis regulating proteins were not associated with patient age , sex , Rai stage , platelet count , hemoglobin ( Hb ) concentration , or lymph node involvement , although higher levels of Bcl 2 and a high Bcl 2 : Bax ratio were correlated with high numbers ( > 10 ( 5 ) / microL ) of white blood cells ( WBC ) ( P = . 01 ; . 007 ) and higher levels of Bak were weakly associated with loss of allelic heterozygosity at 13q14 ( P = . 04 ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Positive ( ICE , ICErel 2 , ICErel 3 , Ich 1L , CPP 32 , mch 2 , mch 3 , bcl xS , bax and bak ) and negative ( bcl 2 , bcl xL , MCL 1 and Ich 1S ) regulators of apoptosis were successively examined using a semi quantitative technique of reverse transcription polymerase chain reaction ( RT PCR ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of the death related proteins ( DRPs ) Bcl 2 , Bax , Bcl 10 and Bak that regulate cell survival and death was examined using immuno histochemical methods in a group of 142 T 1 ( < 2 cm ) ductal breast carcinomas . ^^^ Expression of the apoptotic proteins Bax and Bak was present in 58 % of Bcl 2 negative tumors and associated significantly with an increase in apoptosis . ^^^ Expression of these DRPs was associated significantly with the HG of the tumors : Bcl 2 and Bak expression was predominant in HG I / II tumors , whereas expression of Bcl xL and Bax was commonly observed in HG 3 tumors , as occurs for p 53 over expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cisplatin and paclitaxel induced apoptosis of ovarian carcinoma cells and the relationship between bax and bak up regulation and the functional status of p 53 . ^^^ There were no changes in levels of Bcl 2 , Bcl XL , or 24 kDa Bax over 72 hr after exposure to cisplatin or paclitaxel , but each agent led to up regulation of Bak and 21 kDa Bax in A 2780 cells . ^^^ Paclitaxel , but not cisplatin , increased Bak and 21 kDa Bax levels in A2780 / cp70 cells . ^^^ These data suggest that apoptosis in A 2780 and A2780 / cp70 is associated with an increased level of Bak and 21 kDa Bax after drug induced damage and that functional p 53 may be required for this effect after cisplatin but not after paclitaxel . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak proteins require caspase activity to trigger apoptosis in sympathetic neurons . ^^^ We show that the pro apoptotic proteins Bax and Bak trigger apoptosis when over expressed in sympathetic neurons cultured in the presence of NGF . ^^^ These results demonstrate that in sympathetic neurons Bax and Bak are sufficient to induce apoptosis in the absence of any other apparent cell death stimulus and that their effect is mediated by caspases but does not require reactive oxygen species nor activity of the proteasome . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of p 53 , p21 / WAF / CIP , Bcl 2 , Bax , Bcl 10 , and Bak in radiation induced apoptosis in testicular germ cell tumor lines . ^^^ Expression of p21 / WAF / CIP was determined by Northern blot analysis and immunoblotting was used to monitor p 53 , Bax , Bcl 2 , Bcl 10 , and Bak protein levels . ^^^ Constitutive expression of Bax , Bcl 2 , Bcl 10 , and Bak was not affected by radiation and showed no correlation with cell susceptibility to radiation induced apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Some Bcl 2 related proteins ( Bcl 2 , Bcl xLong , MCl 1 , and Dad 1 ) function as cell death repressors , whereas others ( Bax , Bcl xShort , Bak , and Bad ) facilitate apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Recent studies have focused on the role that programmed cell death ( i . e . , apoptosis ) plays in both normal and neoplastic growth : certain genes can either suppress ( e . g . , Bcl 2 , Bcl xL ) or promote ( e . g . , Bik , Bax , Bak ) apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The results showed no significant difference in the levels of apoptosis inducing proteins bak and bax among all the cell types examined . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Moreover , BI 1 can interact with Bcl 2 and Bcl XL but Bax or Bak , as demonstrated by in vivo cross linking and coimmunoprecipitation studies . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In this study we have investigated by Western blotting the expression pattern of Bcl 2 and its homologues Bax , Bak , Bcl xL , Bcl xS , Mcl 1 and Bad in 12 distant lymph node metastases from patients who have been treated by different regimes , in nine newly established cell lines of these metastases , in three cell lines obtained from other sources and in primary melanocytic cell lines from three neonatal and two adult subjects . ^^^ Taken together , our data suggest that Bax , Bak , Bad , Bcl xL and Mcl 1 are expressed in addition to Bcl 2 in both normal melanocytes and in cell lines established from melanoma metastases . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Second , IFNgamma treatment induced expression of BAK mRNA while MycN and IFNgamma in combination increased the amount of Bax protein , another activator of apoptosis , without a concomitant increase in BAX mRNA . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Quantitative Western blotting was used to examine the protein expression of P 53 and P21WAF 1 , Bcl 2 and Bcl 10 ( L ) ( anti apoptotic proteins ) , and Bax , Bak , and Bad ( proapoptotic proteins ) . ^^^ The results revealed that , upon trophic factor withdrawal , NHP and BPH cells upregulated wild type p 53 and proapoptotic proteins Bax / Bad / Bak and down regulated the expression of P 21 . ^^^ Upon deprivation , these cancer cells up regulated P 21 and Bcl 2 and / or BclX ( L ) , lost response to withdrawal induced up regulation of Bax / Bad / Bak or decreased or even completely lost Bax expression and expressed some novel proteins such as P 25 and P54 / 55 complex . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The present study demonstrates strong expression of bak and bax in the majority of giant cells . ^^^ Only scattered mononuclear cells were positive for bak , bax and bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To investigate the molecular mechanism of glandular parenchyma destruction in Sjgren ' s syndrome ( SS ) , Bcl 2 , Bax , Bcl 10 , and Bak expression were studied . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 family proteins are key regulators of apoptosis and function as cell death antagonists ( e . g . , Bcl 2 , Bcl XL , and Mcl 1 ) or agonists ( e . g . , Bax , Bad , and Bak ) . ^^^ Here we report that among the Bcl 2 family of proteins tested ( Bcl 2 , Bcl XL , Mcl 1 , Bax , Bad , and Bak ) , Bcl XL was unique in that its protein levels were tightly regulated by hemopoietins in both immortal and primary myeloid progenitors . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Formalin fixed tissue sections were immunohistochemically stained for apoptosis associated proteins ( Bcl 2 , Bcl 10 , Bax , Bak , p 53 , MDM 2 , BHRF ) . ^^^ Most lymphomas were positive for Bcl 10 and Bax , and few expressed Bak . ^^^ The irregular expression of Bcl 2 , Bcl 10 , Bax , and Bak in oral lymphomas indicates dysfunctional apoptotic mechanisms in these tumors . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , the bcl 2 related proteins ( bax , bad , and bak ) act by promoting apoptotic cell death as shown from their expression in hematopoietic cell lines . ^^^ Similarly , we analyzed the expression of bcl 2 related proteins bcl xL , bax , bad , and bak before and during ex vivo expansion . ^^^ These cells expressed strongly the bcl xL protein ( > 95 % ) but were bax low ( 4 % to 12 % ) , bad low ( 0 % to 0 . 8 % ) , and bak low ( 0 % to 3 % ) . ^^^ However , the expression of pro and apoptotic antigens increased : bax ( 10 % to 15 % ) , bad ( 5 % to 8 % ) , bak ( 6 % to 14 % ) , and ASP ( 6 % to 10 % ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In the yeast cell assay , BOD interacts with diverse antiapoptotic Bcl 2 proteins [ Mcl 1 , Bcl 2 , Bcl xL , Bcl w , Bfl 1 , and Epstein Barr virus ( EBV ) BHRF 1 ] but not with different proapoptotic Bcl 2 proteins ( BAD , Bak , Bok , and Bax ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
It is , therefore , important to clarify if the Bax protein is limiting for activation of the genetic program of programmed cell death or can be complemented by different Bcl 2 family members , such as Bak or Bad . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bleomycin induced apoptosis was accompanied by decreases in bcl 2 and bcl xl and increases in p 53 , bak , and bax protein levels . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 expression is confined to the base of the colonic crypt , whereas transforming growth factor beta ( TGFbeta ) is expressed in the upper crypt , as are the apoptotic death promoters , Bak and Bax . ^^^ There was no change in the levels of the p 30 phosphorylated form of Bcl 2 or in levels of the proapoptotic proteins Bax or Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 , Bcl 10 ( L ) , Bax , Bad , Bak and p 53 protein expression was analysed by Western blotting . ^^^ LoVo ) , 5 FU induced apoptosis was accompanied by increased expression of Bax and Bak without consistent modulation of other bcl 2 family proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The proteins evaluated were p 53 and six members of the Bax / Bcl 2 family : three proapoptotic proteins ( Bax , Bak , and Bcl xS ) and three survival factors ( Bcl 2 , Bcl xL , and Mcl 1 ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Furthermore , similar deletions for the related channel forming proapoptotic Bax and Bak did not impair their cell killing ability . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of the Bcl 2 , Mcl 1 , Bcl 10 , Bax , and Bak proteins was analyzed to determine whether the differences in MCF 7 cell sensitivity to apoptosis could be correlated to the differential expression of these proteins . ^^^ Whereas Bak , Bcl 10 , and Mcl 1 levels were identical between variants , the levels of Bcl 2 were 3 . 5 3 . 8 fold higher and the levels of Bax were 1 . 5 1 . 7 fold lower in the resistant variants ( M and L ) as compared with those of the sensitive variant ( N ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We have previously examined the involvement of the B cell leukemia 2 gene product ( Bcl 2 ) family proteins ( Bcl 2 , Bcl 10 , Bax , Bak , and Bad ) in Alzheimer ' s disease ( AD ) and found that Bcl 2 , Bcl 10 , Bak , and Bad were upregulated . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Treatment of LNCaP cells with 10 nm Taxol led , after 24 h , to relatively specific and almost total down regulation of bcl xL protein in the absence of alteration of bax , bak , or bcl 2 levels . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Using isolated mitochondria , we found that recombinant Bax and Bak , proapoptotic members of the Bcl 2 family , induced mitochondrial Deltapsi loss , swelling , and cytochrome c release . ^^^ All of these changes were dependent on Ca2+ and were prevented by cyclosporin A ( CsA ) and bongkrekic acid , both of which close the PT pores ( megachannels ) , indicating that Bax and Bak induced mitochondrial changes were mediated through the opening of these pores . ^^^ Proapoptotic Bax and Bak BH 3 ( Bcl 2 homology ) peptides , but not a mutant BH 3 peptide nor a mutant Bak lacking BH 3 , induced the mitochondrial changes , indicating an essential role of the BH 3 region . ^^^ A coimmunoprecipitation study revealed that Bax and Bak interacted with the voltage dependent anion channel , which is a component of PT pores . ^^^ Taken together , these findings suggest that proapoptotic Bcl 2 family proteins , including Bax and Bak , induce the mitochondrial PT and cytochrome c release by interacting with the PT pores . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The talipexole pretreatment induced an increase in antiapoptotic Bcl 2 protein level but had no effect on levels of proapoptotic Bax , Bak , and Bad . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Since the role of the Bcl 2 gene family has been only poorly investigated in colorectal cancer , we have examined the expression of the apoptosis blockers Bcl xL and Bcl 2 , as well as the proapoptotic factors Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of bcl 2 , bcl 10 , bax and bak in renal parenchyma , oncocytomas and renal cell carcinomas . ^^^ Expression of bcl 2 , bcl 10 , bax and bak was investigated by immunohistochemistry and Western blotting of regular and alterated renal parenchyma as well as in 57 renal cell carcinomas . ^^^ Moderate to strong expression for bcl 2 , bcl 10 , bax and bak was found in 24 , 38 , 2 and 13 of 57 carcinomas , respectively . ^^^ Bcl 2 , bcl 10 , bax and bak expression were correlated to tumor type . ^^^ Chromophilic carcinomas stained stronger for bcl 2 , bcl 10 and bax , whereas chromophobic carcinomas stained stronger for bcl 10 , bax and bak compared to clear cell carcinomas . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
During this process , IL 6 downregulated expression of BCL 2 in 1A9 M cells and stimulated BCL XL expression , but had no effect on p 53 , Bax , or Bak gene expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
There was no correlation between the susceptibility to gemcitabine and the endogenous expression of the B cell lymphoma 2 ( BCL 2 ) family proteins BCL 2 , BCL XL , myeloid cell leukemia 1 ( MCL 1 ) , BCL 2 associated 10 protein ( BAX ) , BCL 2 homologous antagonist / killer ( BAK ) and BCL XS . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Nonetheless , there were no significant alterations in levels of immunoreactive Bcl 2 , Bcl 10 ( L ) , Bax , Bad , and Bak , nor any evidence of cytochrome c release into cytosol and dissipation of delta ( psi ) m . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , pro apoptotic members of this family , such as Bax and Bak , trigger the release of caspases from death antagonists via heterodimerization and also by inducing the release of mitochondrial apoptogenic factors into the cytoplasm via acting on mitochondrial permeability transition pore , thereby leading to caspase activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Prognostic significance of Bcl 2 , Bcl xL / S , Bax and Bak expressions in colorectal carcinomas . ^^^ The immunohistochemical expressions of the apoptosis related proteins Bcl 2 , Bcl xL / S , Bax and Bak were investigated in tumor specimens selected from 58 consecutive patients undergoing surgery for advanced colorectal carcinoma . ^^^ In the normal colonic mucosa , Bcl 2 positive epithelial cells tended to be located at the base of the crypts , while the Bcl xL / S , Bax and Bak positive epithelial cells tended to be located at the luminal surface . ^^^ The intracellular expression patterns of Bcl 2 and Bax were diffuse cytoplasmic , whereas those of Bcl xL / S and Bak were granular cytoplasmic . ^^^ In the adenocarcinomas , the intracellular expression patterns of all antibodies were diffuse cytoplasmic , and the percentages of Bcl 2 , Bcl xL / S , Bax and Bak positive cases ( > 20 % of cancer cells labeled ) were 29 % , 43 % , 45 % and 69 % , respectively . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The fivefold elevation in steady state Bcl 2 concentration is not accompanied by detectable changes in the levels or cellular distributions of the related anti apoptotic regulator Bcl xL or of the proapoptotic regulators Bax and Bak and does not produce detectable effects on basal proliferation , differentiation , or death programs . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We used antibodies specific for the human Bcl 2 , Mcl 1 , Bax , Bak and p 53 proteins to examine the expression of these apoptosis regulating genes in 49 archival specimens of patients with radically resected non small cell lung cancer ( NSCLC ) . ^^^ Tumour cells containing immunostaining for the antiapoptotic proteins Bcl 2 and Mcl 1 were present in 31 % and 58 % of the cases evaluated , respectively , whereas immunopositivity for the proapoptotic proteins Bax and Bak was found in 47 % and 58 % of the samples . p 53 immunopositivity was detected in 61 % of the samples . ^^^ Our results establish the frequent expression of the Bcl 2 family proteins Bcl 2 , Mcl 1 , Bax and Bak in NSCLC . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Analysis of Bcl 2 protein family expression in undifferentiated and differentiated cells suggests that susceptibility of M 1 D cells to apoptosis may be controlled , in part , by expression of the proapoptotic alpha isoform of Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
METHODS : Immunohistochemistry was performed on tissue sections using antibodies against bcl 2 , bcl 10 , bax , and bak . ^^^ Both bcl 2 and bax were diffusely cytosolic whereas bcl 10 and bak exhibited a distinct perinuclear distribution . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Certain proapoptotic members of the Bcl 2 family , Bax and Bak , have intrinsic cytotoxic activities in that they not only induce or sensitize mammalian cells to undergo apoptosis but also display a lethal phenotype when ectopically expressed in two yeast species Saccharomyces cerevisiae and Schizosaccharomyces pombe . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Developmental expression patterns of Bcl 2 , Bcl 10 , Bax , and Bak in teeth . ^^^ The ontogenic profile of expression of four members of the Bcl 2 family ( Bcl 2 , Bcl 10 , Bax and Bak ) was examined in the mouse by immunohistochemistry using paraffin sections . ^^^ In general , contemporaneous co expression of the Bcl 2 and Bax proteins , and of the Bcl 10 and Bak proteins was noted in various types of cells during the developmental process , with the intensity of Bcl 2 > Bax and of Bak > Bcl 10 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Here we demonstrate that inhibition of the epidermal growth factor receptor tyrosine kinase activity with either an epidermal growth factor receptor antagonistic monoclonal antibody ( MoAb 425 ) or an epidermal growth factor receptor selective tyrosine kinase inhibitor ( AG 1478 ) downregulated Bcl 10 ( L ) expression in normal human keratinocytes but had no effect on expression of the pro apoptotic Bcl 2 homologs Bad , Bak , and Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of p 53 , Bcl 2 , Mcl 1 , Bax , and Bak was assessed by immunohistochemical analysis . ^^^ RESULTS : Tumor cells containing immunostaining for the antiapoptotic proteins Bcl 2 and Mcl 1 were present in 4 ( 15 % ) and 24 ( 92 % ) of the cases evaluated , respectively , whereas immunopositivity for the proapoptotic proteins Bax and Bak was found in 9 ( 35 % ) and 24 ( 92 % ) of the samples . ^^^ There was a positive correlation between the expression of Bcl 2 and Bax and between Mcl 1 and Bak . ^^^ CONCLUSIONS : Our results establish the frequent expression of the Bcl 2 family proteins Bcl 2 , Mcl 1 , Bax , and Bak in locally advanced head and neck cancer . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We examined the expression of the bcl 2 family oncoproteins bax , bak , bcl 2 , bcl xL , and mcl 1 in the course of differentiation of human keratinocytes cultured at low ( 0 . 15 mM ) and high ( 1 . 87 mM ) calcium concentrations . ^^^ The pro apoptotic bax showed an increase in expression during the first six days of culture , whereas bak remained stable until day 10 when it increased only slightly in both low and high calcium treated cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Ninety archived paraffin embedded specimens from 25 patients ( two or more sequential biopsies each ) and eight control specimens were evaluated in immunohistochemically stained sections for tumor suppressor protein p 53 , p 53 binding protein mdm 2 , and apoptosis regulatory proteins Bcl 2 , Bcl 10 , Bax , and Bak . ^^^ These data show that apoptosis associated proteins are altered in variable patterns in both premalignant and malignant oral epithelial lesions . p 53 and especially Bak and Bcl 10 are expressed early ; Bax is largely absent ; and Bcl 2 and mdm 2 show sporadic expression in the development of oral premalignant and malignant disease . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The Bcl 2 homology 3 ( BH 3 ) domain is crucial for the death inducing and dimerization properties of pro apoptotic members of the Bcl 2 protein family , including Bak , Bax , and Bad . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Epstein Barr virus encodes a novel homolog of the bcl 2 oncogene that inhibits apoptosis and associates with Bax and Bak . ^^^ Furthermore , a recombinant green fluorescent protein BALF 1 fusion protein suppressed apoptosis and associated with Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunostainings for the Bcl 2 family revealed no expression of Bax , Bad or Bak protein in any components , whereas Bcl 2 protein was detected in the periphery of basaloid cell layer , but not in the transitional or shadow cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Thus , the pro apoptotic proteins Bax , Bak and Bad , as well as the death suppressors Bcl 10 , Bcl 2 and Bcl w , are synthesised in mouse mammary gland , and dynamic changes in the expression profiles of these proteins occurs during development . ^^^ In extracts of mammary tissue in vivo , Bak heterodimerized with Bcl 10 whereas Bax associated with Bcl w , but Bak / Bcl w heterodimers were not detected . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Like Bcl 2 , the biochemical mechanism of E1B 19K function includes binding to and antagonization of cellular proapoptotic proteins such as Bax , Bak , and Nbk / Bik . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In selectively vulnerable CNS regions in ALS compared with controls , the proapoptotic proteins Bax and Bak are elevated in the mitochondrial enriched membrane compartment , but are reduced or unchanged in the cytosol . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
There was no evidence showing that changes in the expressions of Bcl 2 , Bcl xL , Bak , and Bax lead directly to IFN alpha mediated apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
METHODS : Primary bovine glomerular endothelial cells were stimulated with TNF alpha or LPS , and apoptotic cell death was investigated by DNA fragmentation analysis , morphological studies , measurement of cytochrome c efflux and mitochondrial permeability transition , Bak , Bad , Bax , Bcl 2 , Bcl xL protein expression , and caspase 3 like protease activity . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Here we create liposomes that carry the mitochondrial porin channel ( also called the voltage dependent anion channel , or VDAC ) to show that the recombinant pro apoptotic proteins Bax and Bak accelerate the opening of VDAC , whereas the anti apoptotic protein Bcl 10 ( L ) closes VDAC by binding to it directly . ^^^ Bax and Bak allow cytochrome c to pass through VDAC out of liposomes , but passage is prevented by Bcl 10 ( L ) . ^^^ In agreement with this , VDAC 1 deficient mitochondria from a mutant yeast did not exhibit a Bax / Bak induced loss in membrane potential and cytochrome c release , both of which were inhibited by Bcl 10 ( L ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , Bcl 2 also prevented the increase in cellular levels of Bak , Bax and Bcl xL , along with degradation of actin and Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunohistochemical analysis of Bcl 2 , Bax , and Bak expression in thyroid glands from patients with subacute thyroiditis . ^^^ To clarify a role of apoptosis and the expression of Bcl 2 family proteins in the pathogenesis of subacute thyroiditis ( SAT ) , we evaluated the expression of Bcl 2 , Bax , and Bak by immunohistochemistry and apoptosis by in situ end labeling of fragmented DNA in thyroid tissues from 11 patients with SAT . ^^^ Bcl 2 , Bak , and Bax were strongly expressed in the granulomas and regenerating thyroid follicular cells from patients with SAT . ^^^ Bcl 2 and Bak , but not Bax , were expressed in follicular cells from normal controls . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To explore further how heterodimerization of opposing members affects survival activity , we have compared the abilities of the anti apoptotic Bcl w and A 1 to bind to the pro apoptotic Bax , Bak , Bad and Bik and to protect cells from their cytotoxic action . ^^^ Bcl w co immunoprecipitated from cell lysates with Bax , Bak , Bad and Bik , but A 1 bound only Bak and Bik . ^^^ Bcl w and A 1 protected against apoptosis induced by over expression of Bax or Bad but not that induced by Bak or Bik . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of the pro apoptotic proteins ( Bax , Bak ) and anti apoptotic proteins ( Bcl 2 , Bcl 10 , Mcl 1 ) was studied by immunohistochemistry in 110 invasive ductal breast carcinomas . ^^^ Overall , Bcl 2 , Bcl 10 , Mcl 1 , Bax , Bak , ER , and p 53 were detected in 62 , 75 , 68 , 75 , 60 , 68 and 26 per cent of the cases respectively , but at different levels in each case . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
No significant changes in Bcl 2 , BclX , and Bax protein expression level were observed in the transfected clones as compared with the control H 460 cells whereas a 2 fold increase in Bak protein levels was noticed . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Mammary gland tissue , similar to many other tissues , expresses a number of different Bcl 2 relatives including bcl 10 , bax , bak , bad , bcl w , bfl 1 , bcl 2 as well as the bcl 2 binding protein Bag 1 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The increased apoptosis in c myc hepatocytes was accompanied by increased p 53 , bax , and bak and decreased bcl 2 protein levels . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In this study , we demonstrate that constitutive expression of bcl xl but not bcl 2 , bcl xs , bak , bad , or bax was associated with apoptosis resistance after IL 2 deprivation in CTLL 2 cells that expressed Tax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The antiapoptotic protein bcl 2 was apparently up regulated in A549 / UCN cells , however , bcl xL , another antiapoptotic protein , was down regulated , without changes in bak and bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expressions of Bcl 2 , Bax and Bak proteins in liver tissues of hepatitis B patients and their significance ] . ^^^ OBJECTIVE : To investigate the expressions of Bcl 2 , Bax and Bak proteins in liver tissues of hepatitis B patients and their relations to apoptosis and necrosis of hepatocytes . ^^^ METHODS : TUNEL assay and immunohistochemistry were used to detect hepatic apoptosis , Bcl 2 , Bax and Bak proteins expressions on hepatocytes respectively . ^^^ There was a positive correlation between degrees of the expression of Bax , Bak and hepatic apoptosis ( P < 0 . 05 ) . ^^^ CONCLUSIONS : The enhanced degrees of the expression of Bax and Bak proteins were accompanied with the enhanced degrees of the necrosis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Unlike other proapoptotic Bcl 2 family members , such as Bax and Bak , Bcl 10 ( S ) does not seem to induce cell death in the absence of an additional death signal . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In order to test the hypothesis that increased apoptotic activity is connected with neuroendocrine differentiation and low differentiation degree in large cell carcinoma ( LCLC ) and is regulated by bcl 2 family proteins , we analysed the extent of apoptosis and tumor necrosis and their relation to the expression of bcl 2 , bax , bak and mcl 1 in 35 LCLCs , of which 20 were classified as large cell neuroendocrine lung carcinomas ( LCNEC ) and 15 as large cell non neuroendocrine lung carcinomas ( LCNNEC ) . ^^^ The extent and intensity of expression of the bcl 2 , bax , bak and mcl 1 proteins were studied by immunohistochemistry . ^^^ Immunohistochemically detected bax , bcl 2 and bak expression was independent of apoptotic index in both tumor types , while there was a statistically significant positive association between mcl 1 expression and apoptotic index in LCNNEC but not in LCNEC . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Our findings show that , similar to Bax , a second apoptosis inducing gene Bak is frequently expressed in Hodgkin ' s disease . ^^^ Moreover , the potential pro apoptotic functions related to Bak and Bax in Hodgkin ' s disease might be surpassed by a stronger expression of anti apoptotic molecules thus explaining tumor progression . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Neither the expression of the anti apoptotic protein Bcl xL nor that of the pro apoptotic proteins Bax and Bak were altered in cells expressing mutated N Ras . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of Bcl 2 and its homologues , Bcl xL , Bcl xS , Bax , Bad , Bak and Bag 1 , was detected in all NHL cases , with wide variations between histological subtypes and within each subtype . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We have found that , in addition to Bcl 2 and Bax , the expression levels of apoptosis inducers ( Bad , Bak ) and inhibitors ( Bcl xL , Mcl 1 ) were highly variable in blasts from 78 children with newly diagnosed acute lymphoblastic leukemia ( ALL ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 , Bcl 10 , Bax , and Bak expression in short and long lived patients with diffuse large B cell lymphomas . ^^^ The expression of the apoptosis regulating proteins , Bcl 2 , Bcl 10 , Bax , and Bak , in the initial biopsy samples was examined with immunohistochemical methods . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Proapoptotic members of the Bcl 2 family , including Bax , Bak , and Bid , directly trigger the mitochondrial release of apoptogenic cytochrome c and apoptosis inducing factor into the cytoplasm . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In the yeast two hybrid system , Mcl 1 binds to the hypophosphorylated mutant of BAD and interacts preferentially with different proapoptotic ( Bax , Bak , Bok , Bik , and BOD ) compared with antiapoptotic Bcl 2 family members ( Bcl 2 , Bcl xL , Bcl w , Bfl 1 , CED 9 , and BHRF 1 ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
L 744 , 832 is capable of inducing apoptosis in astrocytoma cells under anchorage dependent conditions ; this process occurs in a p 53 independent manner and is associated with increased expression of Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Through direct interaction with the voltage dependent anion channel ( VDAC ) , proapoptotic Bcl 2 family members such as Bax and Bak induce apoptogenic mitochondrial cytochrome c release and membrane potential ( Deltapsi ) loss in isolated mitochondria . ^^^ Unlike Bax / Bak , the cytochrome c release induced by Bid / Bik was Ca ( 2+ ) independent , cyclosporin A insensitive , and respiration independent . ^^^ Furthermore , in contrast to Bax / Bak , Bid / Bik neither interacted with VDAC nor directly affected the VDAC activity in liposomes . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , the levels of pro apoptotic Bax and Bak were 3 5 fold higher in the CBL treated A 2780 but not in A 2780 ( 100 ) . ^^^ ETO ( 5 microM ) induced apoptosis in A 2780 without altering the levels of Bax and Bak in these cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of the BCL 2 family proteins , BCL 2 , BAX , BCL ( XL ) and BAK have been determined in a panel of 12 human ovarian carcinoma cell lines encompassing a wide range in sensitivity to cisplatin . ^^^ Whereas BAX , BCL ( XL ) and BAK levels did not correlate with sensitivity , there was a statistically significant inverse correlation ( r = 0 . 81 ; P = 0 . 002 ) between growth inhibition by cisplatin and BCL 2 levels . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Recently , a number of different second messengers ( calcium , ceramide derivatives , nitric oxide , reactive oxygen species ) and pro apoptotic proteins ( Bax , Bak , Bid , and caspases ) have been found to directly compromise the barrier function of mitochondrial membranes , when added to isolated mitochondria . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Platelets aged in vitro not only exhibited increased expression of proapoptotic Bak and Bax but also evidenced constitutive diminution of function such as decreased aggregation to ADP , which was accelerated by culture in the absence of plasma . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We examined the effect of mutant p 53 on camptothecin induced apoptosis and the expression of genes which are known to be involved in apoptosis or drug resistance , such as bcl 2 , bax , bak , p21waf1 , and P glycoprotein . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Using a human lymphoblastoid cell line , we have analysed , following gamma irradiation ( 0 . 5 , 1 , 2 , 4 , 8 , 16 and 32 Gy , at 0 . 5 , 24 , 48 and 72 h after treatment ) , the correlation between proliferation , cell cycle analysis , apoptosis and micronuclei frequency with the expression of TP 53 , WAF 1 , DNA LIGASE 1 , PCNA , BAX , BLC 2 , BAK , DAD 1 , ICH 1 Long and Short forms mRNAs . ^^^ We have found that whereas TP 53 , BAK , ICH 1 Short form , and DAD 1 were expressed at constant levels , WAF 1 , PCNA , BAX were up regulated , ICH 1 Long form , DNA LIGASE 1 , and BCL 2 were down regulated . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Interestingly , 9 cis RA induced transiently the expression of p 21 ( Waf1 / Cip1 ) , p 27 ( Kip 1 ) , p 300 , CBP , BAX , Bak and bcl 2 proteins , respectively . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A Bcl 2 homolog encoded by Kaposi sarcoma associated virus , human herpesvirus 8 , inhibits apoptosis but does not heterodimerize with Bax or Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The authors examined apoptosis and the expression of apoptosis regulating proteins Bcl 2 , Bax , Bak , and Mcl 1 in 21 typical and 10 atypical bronchopulmonary carcinoid tumors . ^^^ METHODS : Thirty one bronchopulmonary carcinoid tumors were examined by using in situ 3 ' end labeling of DNA ( TUNEL ) for apoptosis and immunohistochemical staining methods for Bcl 2 , Bax , Bak , Mcl 1 , p 53 , and Ki 67 in formalin fixed , paraffin embedded tissue specimens . ^^^ No relation between apoptosis and Bcl 2 , Bax , Bak , or Mcl 1 expression was found . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Up regulation of the proapoptotic mediators Bax and Bak after adenovirus mediated p 53 gene transfer in lung cancer cells . ^^^ We observed up regulation of Bax and Bak protein levels 18 36 h after transduction with Adp 53 in H 1299 , H 358 , and H 322 lung cancer cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The BCL 2 family includes both proapoptotic ( e . g . , BAX and BAK ) and antiapoptotic ( e . g . , BCL 2 and BCL 10 ( L ) ) molecules . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We have recently shown that some of these proteins , such as Bcl 10 ( L ) , Bax , and Bak , directly modulate the mitochondrial voltage dependent anion channel ( VDAC ) and thus regulate apoptogenic cytochrome c release and potential loss . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , the expression of Bcl 10 ( L ) decreased and that of proapoptotic Bax , Bad , and Bak was unchanged or down regulated after removal of growth factors . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To investigate the molecular pathway to apoptosis induction , members of the Bcl 2 family of proteins were examined ( Bcl 2 , Bcl 10 , Bax , and Bak ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We first analyzed mRNA expression of pro apoptotic Bak and Bax along with that of anti apoptotic Bcl 2 and Bcl xL , using breast cancer specimens of 27 patients . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl w forms complexes with Bax and Bak , and elevated ratios of Bax / Bcl w and Bak / Bcl w correspond to spermatogonial and spermatocyte apoptosis in the testis . ^^^ Bcl w could form complexes with Bax and Bak but not with Bad . ^^^ Bax and Bak were immunohistochemically localized to the same cell types as Bcl w , but with higher expression levels in spermatocytes and spermatogonia than in Sertoli cells . ^^^ Three animal models that display spermatogonial apoptosis induced by blockade of stem cell factor / c kit interaction by a function blocking anti c kit antibody , spermatocyte apoptosis induced by methoxyacetic acid , and apoptosis of spermatogonia , spermatocytes , and spermatids induced by testosterone withdrawal after ethylene dimethane sulfonate treatment were employed to check the changes of Bcl w , Bax , and Bak protein levels during apoptosis of specific germ cells . ^^^ In all three models , the ratios of Bax / Bcl w and Bak / Bcl w were significantly elevated . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression levels of the tumor suppressor protein , p 53 , the cell cycle inhibitors , p21Waf1 / Cip1 and p27Kip1 , and the pro apoptotic proteins , Bax , Bak , and Bik , were determined . ^^^ Treatment with NaBT was associated with increased expression levels of p21Waf1 / Cip1 p27Kip1 , Bax , Bak , and Bik . ^^^ CONCLUSIONS : NaBT triggers growth arrest and apoptosis in the human gastric cancer SIIA potentially through the induction of the cell cycle inhibitors , p21Waf1 / Cip1 and p27Kip1 , and the proapoptotic genes , Bax , Bak , and Bik . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Using reverse transcriptase polymerase chain reaction , cloning , and sequencing techniques , we have found that HL 60 cells express bak , bik , bax , bad , bcl 2 , bcl xL , bcl w , bfl 1 , fas , and caspases 1 4 and 7 10 . ^^^ Peripheral blood neutrophils expressed bak , bad , bcl w , bfl 1 , fas , and caspases 1 , 3 , 4 , and 7 10 , but hardly expressed bcl 2 , bcl xL , bik , bax , and caspase 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The family can be divided into two classes : those such as Bcl 2 and Bcl xL that suppress cell death , and others , such as Bak and Bax , that appear to promote apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of BCL 2 , BAX and BAK in the trophoblast layer of the term human placenta : a unique model of apoptosis within a syncytium . ^^^ We used immunohistochemistry with monoclonal antisera against human BCL 2 and polyclonal antisera against human BAX and BAK to study paraffin embedded sections of human term placentae ( n=5 ) from uncomplicated pregnancies . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
CONCLUSIONS : The significant increases in the levels of the proapoptotic proteins Bak and Bax and the higher percentage of TUNEL positive cells in both diseased groups suggests the presence of ongoing apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , expression of the proapoptotic proteins Bax and Bak was not significantly influenced by these kinase inhibitors . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The `` Bcl 2 rheostat ' ' may be pitched against apoptosis in colon cancer , inasmuch as overexpression of Bcl 2 , downregulation of Bak , and mutation of Bax are common defects in colon tumors . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The degree of apoptosis was analyzed in relation to several clinicopathologic parameters , cell proliferative activity , and immunohistochemical expression of apoptosis related proteins , including bcl 2 , bax , bcl 10 , bak , p 53 , p 21 ( WAF1 / CIP1 ) , Fas , and Fas ligand . ^^^ Many synovial sarcomas were diffusely positive for bcl 2 family proteins ( bcl 2 , bax , bcl 10 , and bak ) and were negative or only sporadically positive for Fas , Fas ligand , p 53 , and p 21 ( WAF1 / CIP1 ) proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The second part was to investigate the effect of CLA feeding on the development of histologically identifiable premalignant lesions in the rat mammary gland , as well as on the quantification of apoptosis ( by terminal uridyltransferase nick end labeling assay ) and the expression by immunohistochemistry of apoptosis regulatory proteins ( bcl 2 , bak , and bax ) in normal versus premalignant mammary structures . ^^^ It also significantly increased apoptosis and reduced the expression of bcl 2 in these lesions , but it did not modulate the levels of bak or bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To explore the potential involvement of Bcl 2 family members in this process , the expression and localization of some Bcl 2 family proteins ( Bcl 2 , Bcl xL , Bcl w , Bak , Bax , and Bad ) and p 53 were analyzed during testicular development in the rat by Western blotting and immunohistochemistry . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 , Bax , and Bak protein expression in the hepatocytes was determined by immunohistochemistry method . ^^^ RESULTS : No obvious cytotoxicity was noted in 0 . 2 % and 1 % ethanol treatment group , while it developed in 3 % ethanol treatment group and accompanied by a marked expression of Bax , Bak proteins . ^^^ CONCLUSION : The overexpression of Bax , Bak proteins may play a role in HepG ( 2 ) cell apoptosis induced by ethanol and can be blocked effectively by Bcl 2 adenovirus vector . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Levels of the proapoptotic protein Bax remained unchanged during differentiation , while Bak expression doubled within 24 hours . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We found that treatment of MCF 7 cells with Mlt for 24 h before the addition of atRA decreased the protein levels of the death suppressor , Bcl 2 , and increased , although with different time courses , the levels of the death promoters , Bax and Bak ; however , there was no change in the levels of the tumor suppressor gene , p 53 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
RESULTS : Herein , we showed that inhibition of ERK1 / 2 activities caused ( 1 ) a G 1 arrest ; ( 2 ) a down regulation of the expression levels of the anti apoptotic homologs Bcl 2 , Mcl 1 , and Bcl 10 ( L ) without affecting the pro apoptotic levels of Bax and Bak ; ( 3 ) a promotion of caspases 3 , 6 , 8 , and 9 activities ; ( 4 ) a stimulation of PARP cleavage ; and ( 5 ) a programmed cell death by apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Pro apoptotic Bax and Bak have been shown to induce cytochrome c release and loss of membrane potential ( Deltapsi ) leading to AIF release in the isolated mitochondria . ^^^ We have previously shown that Bax and Bak open the voltage dependent anion channel ( VDAC ) allowing cytochrome c to pass through the channel , and Bcl xL closes the channel . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Apoptosis and occurrence of Bcl 2 , Bak , Bax , Fas and FasL in the developing and adult rat endocrine pancreas . ^^^ At each time point , histologic sections were treated with the direct fluorescein labelled TUNEL method and immunostained for pancreatic hormones ( glucagon , insulin ) , apoptotic promoters ( Bak , Bax , Fas , Fas Ligand ) as well as for the anti apoptotic peptide Bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A self contained section concerns itself with the process of programmed cell death ( PCD ) in microorganisms including : 1 ) cell death in the myxomycete Dictyostelium discoideum and the parasitic flagellate Trypanosoma cruzi ; 2 ) PCD in genetically manipulated yeast expressing the proapoptotic Bax and Bak proteins ; 3 ) the death of a part of a prokaryotic cell population upon the depletion of nutrient resources or under stress ; 4 ) the elimination of cells after a loss of a plasmid encoding a stable cytotoxic agent in combination with an unstable antidote ; and 5 ) PCD in phage infected bacterial cells . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
During the leukemic phases , the clonal cells were activated blasts expressing elevated levels of wild type ( wt ) p 53 , Bcl 2 , Bcl 10 ( L ) , and Bax , while Bak expression increased during the decline of lymphocytosis . ^^^ The data suggest that wt p 53 , Bcl 10 ( L ) , and Bcl 2 / Bax heterodimers support the accumulation of activated leukemic cells during the leukemic phases , while Bax and Bak may be involved in their decline during regression . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , levels of Bax protein remained relatively unchanged in four of the cell lines , and levels of Bcl 10 ( L ) , Bcl 10 ( S ) , and Bak proteins showed little or no cell cycle dependent changes in Jurkat T cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunoblotting experiments demonstrated no difference in the expression of the pro apoptotic factors Bax , Bad , and Bak in either control U 937 and TPA treated adherent or suspension cells , respectively . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
There was no correlation between expression of members of the Bcl 2 family ( Bcl 2 , Bcl xL , Bax , and Bak ) and TRAIL sensitivity . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
After PDT , expression of Bcl 2 , Bcl 10 ( L ) , Bax , and Bak was also examined in cell lysates by Western blot analysis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
TSA enhanced the protein expression of p 21 ( WAF 1 ) , CREB binding protein , cyclinE , cyclin A , Bak and Bax , while it reduced the expression of E2F 1 , E2F 4 , HDAC 1 , p 53 and hyperphosphorylated form of Rb . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Yeast and other simple eukaryotes contain components of a proapoptotic pathway which are silent under normal conditions but can be activated by oxidative stress or by manifestation of mammalian death genes , such as bak or bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Role of Bcl 2 , Bax , and Bak in spontaneous apoptosis and proliferation in neuroendocrine lung tumors : immunohistochemical study . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Adult mice exposed to greater than 95 % oxygen concentrations for 48 to 88 hours had increased whole lung mRNA levels of Bax and Bcl 10 ( L ) , no change in Bak , Bad , or Bcl 2 , and decreased levels of Bcl w and Bfl 1 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Both anti apoptotic ( Bcl W , Bcl 10 ( L ) ) and pro apoptotic ( Bad , Bak , Bax ) members of the Bcl 2 family were expressed in developing skeletal muscle in vivo . ^^^ Loss of Bcl 2 did not affect expression of other family members , because neonatal muscles of wild type and Bcl 2 null mice had similar amounts of Bcl 10 ( L ) , Bcl W , Bad , Bak , and Bax mRNAs . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The combined functions of proapoptotic Bcl 2 family members bak and bax are essential for normal development of multiple tissues . ^^^ However , when Bak deficient mice were mated to Bax deficient mice to create mice lacking both genes , the majority of bax ( / ) bak ( / ) animals died perinatally with fewer than 10 % surviving into adulthood . bax ( / ) bak ( / ) mice displayed multiple developmental defects , including persistence of interdigital webs , an imperforate vaginal canal , and accumulation of excess cells within both the central nervous and hematopoietic systems . ^^^ Thus , Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
After 6 days of 9CRA treatment , RARbeta transfectants overexpressed Waf 1 / Cip 1 / Sdi 1 / p 21 , Kip 1 / p 27 , chk 1 , p 300 / CBP , BAX , Bak , Apaf 1 , caspase 3 and caspase 9 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Pro apoptotic cascade activates BID , which oligomerizes BAK or BAX into pores that result in the release of cytochrome c . ^^^ In parallel , the full pro apoptotic member BAX , which is highly homologous to BAK , rapidly forms pores in liposomes that release intravesicular FITC cytochrome c approximately 20A . ^^^ Thus , an activation cascade of pro apoptotic proteins from BID to BAK or BAX integrates the pathway from surface death receptors to the irreversible efflux of cytochrome c . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Overexpression of mda 7 protein by Ad mda 7 significantly suppressed proliferation and induced G2 / M cell cycle arrest in wild type p 53 ( A 549 , H 460 ) , and p 53 null ( H 1299 ) non small cell lung cancer cell lines , but not in normal human lung fibroblast ( NHLF ) cells . p 53 , Bax , and Bak protein expression was up regulated in wild type p 53 tumor cell lines , but not in p 53 null cells , suggesting that an intact p 53 pathway was required for Bax and Bak induction . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Progress has been made especially in the elucidation of the mechanisms of action of the Bcl 2 family members , in detail the formation of channels and their regulation in the mitochondrial membranes , conformational changes in Bax and Bak , and crosstalk of death receptor triggered apoptosis to the mitochondria by activation of Bax via Bid . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Since the Bcl 2 family of proteins constitutes a critical checkpoint in apoptosis , acting upstream of the apoptotic machinery , we investigated the expression of six Bcl 2 homologs ( Bcl 2 , Bcl 10 ( L ) , Mcl 1 , Bax , Bak , Bad ) and one non homologous associated molecule ( Bag 1 ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The sensitivity of the cells to thapsigargin induced apoptosis was evaluated by cell viability and nuclear fragmentation ( Hoechst 33258 ) and compared with pro ( Bcl 2 , Bcl 10 ( L ) ) and anti apoptotic ( Bax , Bak ) protein expression of the Bcl 2 family . ^^^ Bax and Bak expression were not significantly modified . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of proapoptotic ( Bad , Bak , Bax ) and antiapoptotic ( Bcl 2 , Bcl XL ) genes was analyzed by quantitative RT PCR . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
METHODS : We induced mouse liver injury with TNF alpha and D galactosamine , and detected hepatic apoptosis , the expression of Bcl 2 , Bax , and Bak proteins on hepatocytes by using TUNEL or immunohistochemistry , respectively . ^^^ RESULTS : Hepatocyte apoptosis was induced in BalB / c mice pretreated with TNF alpha plus D galactosamine , accompanying the enhanced expression of Bax , Bak proteins in hepatocytes . ^^^ CONCLUSIONS : The enhanced expression of Bax , Bak proteins may play a role in hepatocyte apoptosis induced by TNF alpha and D galactosamine . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In both PEM and J 774 cells , mRNA expression of the anti apoptotic gene , A 1 , was selectively induced by BCG treatment as compared with other bcl 2 family members ( bcl w , bcl 2 , bcl xl , bcl xs , bax , bak , bad ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
No interaction of Bcl rambo with either anti apoptotic ( Bcl 2 , Bcl 10 ( L ) , Bcl w , A 1 , MCL 1 , E1B 19K , and BHRF 1 ) or pro apoptotic ( Bax , Bak , Bik , Bid , Bim , and Bad ) members of the Bcl 2 family was observed . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Through direct interaction with the voltage dependent anion channel ( VDAC ) , proapoptotic members of the Bcl 2 family such as Bax and Bak induce apoptogenic cytochrome c release in isolated mitochondria , whereas BH 3 only proteins such as Bid and Bik do not directly target the VDAC to induce cytochrome c release . ^^^ Furthermore , we used these antibodies to show that Bax and Bak induced lysis of red blood cells was also mediated by the VDAC on plasma membrane . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The effects of Bcl 2 expression on cellular proliferation , cell death ( + / adriamycin or thapsigargin ) , and expression of cell cycle / death regulators ( p 53 , PCNA , Bax , Bak , Bcl 10 ( L ) ) were evaluated . ^^^ Compared with controls , Bcl 2 transfectants showed no difference in the rate of proliferation , a decrease in p 53 ( approximately two fold ) , an increase in Bax ( approximately two fold ) and PCNA ( approximately three fold ) , and no change in the levels of Bcl 10 ( L ) and Bak proteins . ^^^ In the presence of thapsigargin or adriamycin , levels of Bcl 2 and its heterodimeric partner Bax were elevated approximately two fold with no change in Bak in Bcl 2 transfectants in contrast to controls , where Bak was increased ( two fold ) . ^^^ Moreover , Bcl 2 overexpression conferred a significant cytotoxic chemoresistance and altered the balance of expression of death promoters ( from Bak , a dominant death promoter in controls , to Bax ) in response to thapsigargin and adriamycin . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl B , a novel Bcl 2 family member that differentially binds and regulates Bax and Bak . ^^^ The Bcl B protein binds Bcl 2 , Bcl 10 ( L ) , and Bax but not Bak . ^^^ In transient transfection assays , Bcl B suppresses apoptosis induced by Bax but not Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Furthermore , TGF beta had no direct effect on levels of mRNA for members of the bcl family ( bcl 10 , bfl 1 , bik , bak , bax , bcl 2 and mcl 1 ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
GnRH Bik / Bax / Bak chimeric proteins target and kill adenocarcinoma cells ; the general use of pro apoptotic proteins of the Bcl 2 family as novel killing components of targeting chimeric proteins . ^^^ Sequences encoding the human Bik , Bak or Bax proteins were fused to the GnRH coding sequence at the DNA level and were expressed in E . coli . ^^^ GnRH Bik , GnRH Bak and GnRH Bax new chimeric proteins efficiently and specifically inhibited the cell growth of adenocarcinoma cell lines and eventually led to cell death . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Proliferation ( Ki 67 ) , p 53 , BCL 2 , MCL 1 , BAX and BAK protein expression were evaluated by immunohistochemistry . ^^^ A positive correlation existed between mRNA expression of hTERT , hTER and Tankyrase . hTERT mRNA expression tended to be higher with increasing levels of apoptosis and proliferation , in HG NHL samples lacking BAX expression and in samples from patients with survival shorter than 3 . 5 years . hTER mRNA expression was significantly higher in BAX and BAK negative samples . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The ricin induced apoptosis of BEL 7404 was accompanied by increased expression of Bak and decreased levels of Bcl xl and Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Proapoptotic BAX and BAK : a requisite gateway to mitochondrial dysfunction and death . ^^^ Multiple death signals influence mitochondria during apoptosis , yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear . tBID , the caspase activated form of a `` BH 3 domain only ' ' BCL 2 family member , triggers the homooligomerization of `` multidomain ' ' conserved proapoptotic family members BAK or BAX , resulting in the release of cytochrome c from mitochondria . ^^^ We find that cells lacking both Bax and Bak , but not cells lacking only one of these components , are completely resistant to tBID induced cytochrome c release and apoptosis . ^^^ Thus , activation of a `` multidomain ' ' proapoptotic member , BAX or BAK , appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In the present study , we approached this by investigating the expression of six Bcl 2 homologs ( Bcl 2 , Bcl XL , Mcl 1 , Bax , Bak , Bad ) , and one nonhomologous associated molecule ( Bag 1 ) , during development of the human ileum and colon ( 12 20 wks of gestation ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Because cisplatin induced modulation of the related Bax protein was seen in only one cell line , a degree of specificity in the signal to Bak is indicated . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
PURPOSE : We investigated the association of the apoptosis related proteins Bcl 2 , Bcl 10 , Bax and Bak , p 53 , the adhesion molecule E cadherin , the receptor proteins epidermal growth factor receptor and c erbB 2 , and the proliferation markers proliferating cell nuclear antigen and Ki 67 with the clinical outcome of bilharzial related transitional cell carcinoma and squamous cell carcinoma . ^^^ RESULTS : In squamous cell carcinoma but not in transitional cell carcinoma the loss of epidermal growth factor receptor , Bax and Bak was significantly associated with higher histological grade ( p = 0 . 02 , 0 . 006 and 0 . 01 , respectively ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , relative expression levels of six Bcl 2 homologs ( Bcl 2 , Bcl 10 ( L ) , Mcl 1 , Bax , Bak , and Bad ) and activation levels of Fak , Erk 2 , and Akt were analyzed . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Other Bcl 2 family proteins , including Bax ( a heterodimerization partner of Bcl 2 ) , Bcl XL , Bak and Bad , were expressed , but at constant levels . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Levels of Bax , Bid , and Bak proteins were similar in all lines , but levels of Bcl 2 were lower in MCF 10AT and MCF 10ATG3B cells than in MCF A cells , and Bcl 2 Bax heterodimerization progressively declined in the series . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Apoptosis in cultured rat islets of langerhans and occurrence of Bcl 2 , Bak , Bax , Fas and Fas ligand . ^^^ At designated intervals , histologic sections were treated with the direct fluorescein labelled TUNEL method and immunostained for pancreatic hormones ( glucagon , insulin ) and apoptotic peptides [ Bak , Bax , Fas , Fas ligand ( FasL ) ] , as well as for the anti apoptotic peptide Bcl 2 . ^^^ Corresponding cells often contained Bak and Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak coalesce into novel mitochondria associated clusters during apoptosis . ^^^ Bak , a close homologue of Bax , colocalizes in these apoptotic clusters in contrast to other family members , Bid and Bad , which circumscribe the outer mitochondrial membrane throughout cell death progression . ^^^ We found the formation of Bax and Bak apoptotic clusters to be caspase independent and inhibited completely and specifically by Bcl 10 ( L ) , correlating cluster formation with cytotoxic activity . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
BH 3 only proteins that bind pro survival Bcl 2 family members fail to induce apoptosis in the absence of Bax and Bak . ^^^ The BH 3 only proteins Bim and Bad bind to the antiapoptotic Bcl 2 proteins and induce apoptosis in wild type cells and cells from either bax ( / ) or bak ( / ) animals . ^^^ In contrast , constitutively active forms of Bim and Bad failed to induce apoptosis in bax ( / ) bak ( / ) cells . ^^^ In addition , Bax but not Bim or Bad sensitized the bax ( / ) bak ( / ) cells to a wide variety of cell death stimuli including UV irradiation , chemotherapeutic agents , and ER stress . ^^^ These results suggest that neither activation of BH 3 only proteins nor suppression of pro survival Bcl 2 proteins is sufficient to kill cells in the absence of both Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The block in the apoptotic cascade was in the mitochondrial mechanism for cytochrome c release because purified mitochondria from Bak deficient cells failed to release cytochrome c or apoptosis inducing factor in response to recombinant Bax or truncated Bid . ^^^ Following mitochondrial localization , low dose recombinant Bak restored the mitochondrial release of cytochrome c in response to Bax ; at increased doses it induced cytochrome c release itself . ^^^ The function of Bak is independent of Bid and Bax because recombinant Bak induced cytochrome c release from mitochondria purified from Bax ( / ) , Bid ( / ) , or Bid ( / ) Bax ( / ) mice . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
METHODS AND RESULTS : For immunohistochemistry , tissue sections of 32 patients were treated with an antigen retrieval METHOD : Primary antibodies against the apoptosis related proteins , bcl 2 , bcl 10 , bax , and bak were applied . ^^^ Most of the outer layer cells were predominantly stained by the bcl 2 antibody , while most of the inner layer cells were stained by antibodies against the apoptosis modulating proteins , bax and bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Levels of the apoptosis regulating proteins ( BCL 2 , BAK , and BAX ) were determined by Western blotting . ^^^ RESULTS : PS 341 decreased BCL 2 , without effect on BAX or BAK . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Additionally , U 69593 increased the content of the anti apoptotic members of the Bcl 2 family of proteins , the Bcl 2 and Bcl 10 ( L ) , whereas it had no significant effect on the apoptosis promoting homologues Bax , Bcl 10 ( S ) and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Emodin induced apoptosis of CH 27 cells does not involve modulation of endogenous Bcl 10 ( L ) protein expression , but appears to be associated with the increased expression of cellular Bak and Bax proteins . ^^^ This study also demonstrated the translocation of Bak and Bax from cytosolic to particulate fractions . 4 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Using mid gestation human jejunum and colon organotypic cultures , we analyzed the impact of growth factors ( namely insulin ; 10 microg / ml ) and pharmacological compounds that inhibit signal transduction molecules / pathways ( namely tyrosine kinases , Fak , P 13 K / Akt , and MEK / Erk ) on cell survival and Bcl 2 homolog expression ( anti apoptotic : Bcl 2 , Bcl 10 ( L ) , Mcl 1 ; pro apoptotic : Bax , Bak , Bad ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Non steroidal anti inflammatory drugs induce apoptosis in gastric cancer cells through up regulation of bax and bak . ^^^ The pro apoptotic proteins bax and bak were overexpressed after treatment , while the protein level of bcl 2 remained unchanged . ^^^ Our results suggest that one of the major pathways which mediates the anti tumour response of aspirin and indomethacin in gastric cancer cells is through up regulation of bax and bak and activation of caspase 3 . ^^^ Bax and bak are important in the chemoprevention of gastric cancer . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Prognostic value of p 53 , p21 / WAF1 , Bcl 2 , Bax , Bak and Ki 67 immunoreactivity in pT 1 G3 urothelial bladder carcinomas . pT 1 G3 bladder carcinomas are heterogeneous with respect to tumor recurrence and progression . ^^^ Our goal was to determine the prognostic value of p 53 , p21 / WAF1 , Bcl 2 , Bax , Bak , and Ki 67 immunoreactivity in these tumors . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Terminal deoxynucleotidyl transferase mediated dUTP nick end labeling and DNA laddering studies demonstrated that cardiomyocyte apoptosis was attenuated in IL 1ra transfected hearts ( 21 . 4+ / 3 . 3 versus 41 . 4+ / 3 . 4 % , P=0 . 002 ) , correlating with reduced post I / R upregulation of Bax , Bak , and caspase 3 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Tumor necrosis factor alpha induces Bax Bak interaction and apoptosis , which is inhibited by adenovirus E1B 19K . ^^^ TNF alpha signaling induced Bak Bax interaction and both Bak and Bax oligomerization . ^^^ E1B 19K was constitutively in a complex with Bak , and blocked the Bak Bax interaction and oligomerization of both . ^^^ Since either Bax or Bak is essential for death signaling by TNF alpha , the interaction between E1B 19K and both Bak and Bax may be required to inhibit their cooperative or independent oligomerization to release proteins from mitochondria which promote caspase activation and cell death . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Following AdBax / SB and AdBak / SB , a decrease of the AAP bcl xl was noted in combination with increases in PAP bax and bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
BCL 2 , BCL 10 ( L ) sequester BH 3 domain only molecules preventing BAX and BAK mediated mitochondrial apoptosis . ^^^ Cells with an upstream defect , lacking `` multidomain ' ' BAX , BAK demonstrate long term resistance to all BH 3 domain only members , including BAD , BIM , and NOXA . ^^^ Comparison of wild type versus mutant BCL 2 , BCL 10 ( L ) indicates these antiapoptotics sequester BH 3 domain only molecules in stable mitochondrial complexes , preventing the activation of BAX , BAK . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Taking advantage of the human apoptosis inducing proteins Bak and Bax as novel killing components , we have now constructed new chimeric proteins targeted against the human FcepsilonRI , expressed mainly on mast cells and basophils . ^^^ Treatment of the target cells with the new chimeric proteins , termed Fcepsilon Bak / Bax , had a dramatic effect on cell survival , causing apoptosis . ^^^ Fcepsilon Bak / Bax are new chimeric proteins of human origin and , as such , are expected to be both less immunogenic and less toxic and , thus , may be specific and efficient reagents for the treatment of allergic diseases . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
DMS inhibited bcl 10 ( L ) and bak but not bax gene expression , while BSOCOP potentiated bax mRNA synthesis immediately after application . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunohistochemical expression of p 53 , p21 / waf1 , rb , p 16 , cyclin D 1 , p 27 , Ki 67 , cyclin A , cyclin B 1 , bcl 2 , bax and bak proteins and apoptotic index in normal thymus . ^^^ The immunohistochemical expression of p 53 , p 21 , Rb , p 16 , cyclin D 1 , Ki 67 , cyclin A , cyclin B 1 , p 27 , bcl 2 , bax , and bak proteins and the apoptotic index ( Al ) were investigated in 20 normal thymuses ( 8 adults , 3 adolescents , 5 infants and 4 newborns ) . ^^^ The expressions of Bax and bak were more widespread in both the medulla and cortex , suggesting that these proteins play a broader role than bcl 2 in the regulation of thymic apoptosis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
After neutrophils were incubated with HPWE , expression of Bcl 2 family [ antiapoptotic ( Bcl 2 , Bcl XL and Mcl 1 ) and proapoptotic ( Bax , Bak and Bcl XS ) ] was determined by RT PCR and Western blotting , respectively . ^^^ The expression of Bax and Bak was upregulated and Bcl 2 , Bcl XL and Mcl 1 downregulated in HL 60 cells during neutrophilic differentiation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Protein levels for the proapoptotic proteins Bad , Bax , Bak , and Bik remained constant during culture , despite changes in the levels of mRNA for these gene products . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Sparse motor neurons were immunoreactive for bcl 2 , bax , bak , and CM 1 on serial sections through the spinal cord and motor cortex of individual sALS patients and controls . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A significant decrease in BCL XL protein expression was noted with BAK , BAX , and BCL 2 unchanged , and this was corroborated at the transcriptional level with selectively decreased bcl xl mRNA production after sodium butyrate exposure . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Importantly , 16 10A1 could retard the growth of lymphomas and favored the up regulation of pro apoptotic molecules caspase 3 , caspase 8 , Fas , FasL , Bak , and Bax and down regulation of anti apoptotic molecule Bcl 10 ( L ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Aloe emodin induced apoptosis of CH 27 cells involved modulation of the expression of Bcl 2 family proteins , such as BclX ( L ) , Bag 1 , and Bak , and was associated with the translocation of Bak and Bax from cytosolic to particulate fractions . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax , Bak , Bcl 2 , caspases and p 53 ) have been identified in a unicellular eukaryote , previous reports contain several implications of the apoptotic behaviour of yeasts ( i . e . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The proapoptotic protein , Bak , was not detected in HepG 2 cells and O2 * induced CCR did not depend on Bax translocation to mitochondria . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak promote apoptosis by modulating endoplasmic reticular and mitochondrial Ca2+ stores . ^^^ Here we report that enforced expression of either Bax or Bak via adenoviral gene delivery results in the accumulation of the proteins in the endoplasmic reticulum ( ER ) and mitochondria , resulting in early caspase independent BCL 2 sensitive release of the ER Ca ( 2+ ) pool and subsequent Ca ( 2+ ) accumulation in mitochondria . ^^^ Bax and Bak also directly sensitize mitochondria to cytochrome c release induced by immediate emptying of ER Ca ( 2+ ) pool . ^^^ Our results demonstrate that the effects of the `` multidomain ' ' proapoptotic BCL 2 family members Bak and Bax involve direct effects on the endoplasmic reticular Ca ( 2+ ) pool with subsequent sensitization of mitochondria to calcium mediated fluxes and cytochrome c release . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In comparison , strong expression of Bax , Bak and p 21 ( waf1 / cip1 ) and suppressed expression of Bcl 2 , Bcl 10 ( L ) and COX 2 were observed in the Mn SOD antisense group and the expression pattern of these proteins was the inverse in the empty vector group . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Granzyme B can cause mitochondrial depolarization and cell death in the absence of BID , BAX , and BAK . ^^^ Although GzmB directly cleaves the Bcl 2 family member BID on target cell entry , Bid deficient ( and Bax , Bak doubly deficient ) cells are susceptible to GzmB induced death , even though they fail to release cytochrome c from mitochondria . ^^^ GzmB still induces mitochondrial depolarization in Bax , Bak double knockout cells without cytochrome c release or opening of the permeability transition pore . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We show that BAX and BAK , two closely related death promoting members of the BCL 2 family , are expressed in Sertoli cells . ^^^ To determine whether either BAX or BAK activity is required for Sertoli cell death in Bclw mutant animals , we analyzed survival of Sertoli cells in Bclw / Bax and Bclw / Bak double homozygous mutant mice . ^^^ While mutation of Bak had no effect , ablation of Bax suppressed the loss of Sertoli cells in Bclw mutants . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Overexpression of the apoptosis promoting Bax homologue Bak or the BH 3 only protein Nbk / Bik reverts , as expected , acquired drug resistance in the MT 1 Adr cells as recently demonstrated for pro caspase 3 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Activation of the tumor necrosis factor R1 / Fas receptor results in the cleavage of cytosolic BID to truncated tBID . tBID translocates to the mitochondria to induce the oligomerization of BAX or BAK , resulting in the release of cytochrome c ( Cyt c ) . ^^^ Here we demonstrate that in tumor necrosis factor alpha activated FL5 . 12 cells , tBID becomes part of a 45 kDa cross linkable mitochondrial complex that does not include BAX or BAK . ^^^ Surprisingly , enforced dimerization of tBID did not result in the dimerization of either BAX or BAK . ^^^ Moreover , a tBID BH 3 mutant ( G94E ) , which does not interact with or induce the dimerization of either BAX or BAK , formed the 45 kDa complex and induced both Cyt c release and apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We evaluated the expression of apoptosis regulating proteins ( p 53 , Bcl 2 , Bax , Bak and Mcl 1 ) in paraffin embedded tissues of 33 patients with diffuse large B cell non Hodgkin ' s lymphoma , and assessed the relationship of these proteins to clinical outcome and response to chemotherapy . ^^^ Bcl 2 , Bax , Bak and Mcl 1 proteins , though highly expressed in almost all cases were not associated with prognosis or response to treatment . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The regulatory proteins Bcl 2 , Bax , and Bak constitute a diffusion driven molecular switch with inherent damping of apoptosis induction , thereby controlling the apoptosis reaction cascade under noisy , external apoptosis inducing conditions . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak independently promote cytochrome C release from mitochondria . ^^^ Pro apoptotic Bax and Bak have been implicated in the regulation of p 53 dependent apoptosis . ^^^ We assessed the ability of primary baby mouse kidney ( BMK ) epithelial cells from bax ( / ) , bak ( / ) , and bax ( / ) bak ( / ) mice to be transformed by E1A alone or in conjunction with dominant negative p 53 ( p53DD ) . ^^^ Although E1A alone transformed BMK cells from p 53 deficient mice , E1A alone did not transform BMK cells from bax ( / ) , bak ( / ) , or bax ( / ) bak ( / ) mice . ^^^ Thus , the loss of both Bax and Bak was not sufficient to relieve p 53 dependent suppression of transformation in epithelial cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , Bcl 2 hyperphosphorylation ; increase in the proapoptotic proteins Bax , Bak , and Bad ; and Bad hypophosphorylation occurred in the antisense treated cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Dynamics of expression of apoptosis regulatory proteins Bid , Bcl 2 , Bcl 10 , Bax and Bak during development of murine nervous system . ^^^ We have used immunohistochemistry and immunoblotting to examine the expression of Bid and four other Bcl 2 family proteins ( Bcl 2 , Bcl 10 , Bax and Bak ) in the developing and adult murine central nervous system ( CNS ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Infection of metastatic melanoma cells with Ad . mda 7 results in an increase in cells in the G ( 2 ) / M phase of the cell cycle and changes in the ratio of pro apoptotic ( BAX , BAK ) to anti apoptotic ( BCL 2 , BCL XL ) proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Apoptotic signaling by p 53 induced a Bid independent conformational change in Bax , a Bax Bak interaction , release of cytochrome c and Smac / DIABLO from mitochondria , caspase 9 and 3 activation , cleavage of known caspase substrates , and apoptosis . ^^^ When p 53 dependent apoptosis was blocked by E1B 19K expression , E1B 19K bound Bak , and the Bax Bak interaction was inhibited . ^^^ Thus , p 53 induces apoptosis in part through Bax and Bak , and even an incomplete inhibition of this mitochondrial checkpoint may be sufficient to confer resistance to cell death . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of Bcl 2 family proteins ( Bcl 2 , Bcl 10 , Bax , Bak and Bim ) in human lymphocytes . ^^^ We investigated the expression of Bcl 2 , Bcl 10 , Bax , Bak and Bim in human lymphocytes using flow cytometry . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of Bcl 10 , Bcl 2 , Bax , and Bak in endarterectomy and atherectomy specimens . ^^^ The aim of this study was to determine the expression of Bcl 2 , Bcl 10 , Bax , and Bak in relation to apoptosis in advanced atherosclerotic lesions . ^^^ In all TUNEL positive apoptotic cells , Bax and Bak were present , while Bcl 10 was absent . ^^^ In conclusion , increased Bax and Bak coupled with lack / paucity of Bcl 2 and Bcl xL are associated with SMC apoptosis in advanced lesions . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Murine embryonic fibroblasts from bax ( / ) bak ( / ) mice exposed to nitric oxide during hypoxia did not die , indicating that pro apoptotic Bcl 2 family members are required for NO induced apoptosis during hypoxia . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of Bcl 2 , Bcl 10 , Mcl 1 , Bax and Bak in human uterine leiomyomas and myometrium during the menstrual cycle and after menopause . ^^^ To investigate the expression of Bcl 2 , Bcl 10 , Mcl 1 , Bax and Bak proteins in human uterine leiomyomas and homologous myometrium during the menstrual cycle and after menopause . ^^^ The expression of Bcl 2 , Bcl 10 , Mcl 1 , Bax and Bak in leiomyomas ( n=24 ) and myometrial samples ( n=22 ) from women with leiomyomas was measured by immunohistochemistry and Western blot . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Chemotherapeutic agents upregulated expression of the Apo2L / TRAIL receptor DR 5 and the Bax homolog Bak in Baxminus sign / minus sign cells , and restored Apo2L / TRAIL sensitivity in vitro and in vivo . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Rat1a cells exposed to hyperoxia underwent apoptosis characterized by the release of cytochrome c , activation of caspase 9 , and nuclear fragmentation that was prevented by the overexpression of Bcl 10 ( L . ) Murine embryonic fibroblasts from bax ( / ) bak ( / ) mice were resistant to hyperoxia induced cell death . ^^^ We conclude that exposure to hyperoxia results in apoptosis that requires Bax or Bak and can be prevented by the overexpression of Bcl 10 ( L ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bid is the only known Bcl 2 family member that can function as an agonist of proapoptotic Bcl 2 related proteins such as Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In patients with untreated CD there was a 2 . 3 fold higher expression of Bak mRNA ( p = 0 . 026 ) , without significant differences in the expression of related genes bax or bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Levels of an anti apoptotic NF kappaB target , Bcl 2 , were increased fourfold whereas proapoptotic proteins Bax and Bak decreased . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunoblotting was used to evaluate the following in proteins : poly ( ADP ribose ) polymerase ( PARP ) , caspases 8 and 3 , Bcl 2 , heat shock protein ( HSP ) 70 , Bax , Bak and Stat 1 ( a protein known to be inducible by IFN gamma ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 family member Bfl 1 / A1 sequesters truncated bid to inhibit is collaboration with pro apoptotic Bak or Bax . ^^^ However , Bfl 1 remains tightly and selectively bound to tBid and blocks collaboration between tBid and Bax or Bak in the plane of the mitochondrial membrane , thereby preventing mitochondrial apoptotic activation . ^^^ Lack of demonstrable interaction between Bfl 1 and Bak or Bax in the mitochondrial membrane suggests that Bfl 1 generally prevents the formation of a pro apoptotic complex by sequestering BH 3 domain only proteins . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bak and Bax function to limit adenovirus replication through apoptosis induction . ^^^ Unlike apoptosis mediated by death receptors , infection with proapoptotic E1B 19K mutant viruses did not induce cleavage of Bid but nonetheless induced changes in Bak and Bax conformation , Bak Bax interaction , caspase 9 and 3 activation , and apoptosis . ^^^ In wild type adenovirus infected cells , in which E1B 19K inhibits apoptosis , E1B 19K was bound to Bak , precluding Bak Bax interaction and changes in Bax conformation . ^^^ Infection with E1B 19K mutant viruses induced apoptosis in wild type and Bax or Bak deficient baby mouse kidney cells but not in those deficient for both Bax and Bak . ^^^ Furthermore , Bax and Bak deficiency dramatically increased E1A expression and virus replication . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Although protein expression of Fas , FADD , Bax , Bak , and Bcl 10 in the whole cell lysates was not changed by H pylori , Bax was decreased from mitochondria free cytosol suggesting that Bax was translocated into mitochondria . ( 3 ) Cell death and the activities of caspases 3 and 8 were promoted in MKN 45 cells stably expressing super repressor Ikappabetaalpha that inhibits NFkappaB activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We searched for immunoreactivity of glial cells for the apoptotic related markers death receptor ( DR ) 3 , Bax and Bak , the anti apoptotic marker Bcl 2 and the cell cycle marker Ki 67 . ^^^ The pro apoptotic markers Bax , Bak and DR 3 were all modestly increased in glial cell cytoplasm in CPM , while there was no change in expression of Bcl 2 , which was only sparsely detected in glial cells both in controls and cases of CPM . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Mice lacking the proapoptotic Bax and Bak genes were not able to release cytochrome c from the mitochondrion and were blocked in apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Interestingly , Bimgamma mRNA , similar to the BimEL protein , is up regulated in the majority of the prostate cancer cell lines studied , whereas several other proapoptotic Bcl 2 proteins , including Bax , Bak , and Bad , are down regulated in prostate cancer cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Either of these events represses the function of the pro apoptotic proteins Bax and Bak , which are required for mitochondrial release of cytochrome c . ^^^ As we discuss here , the apparently redundant functions of Bax and Bak may have evolved to prevent lymphocyte mitochondria from adapting to loss of receptor mediated signal transduction and thus keep lymphocytes from accumulating in a cell autonomous manner . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
RESULTS : The mucosal tissues of the ulcer site had substantially higher contents of sFasL and IFN gamma in organ cultures regardless of its healing stage in association with increased numbers of apoptotic cells and enhanced expression of proapoptotic proteins Bak and Bax in the surface foveolar epithelium as compared with the antral tissues in patients with H . pylori positive GU . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Therefore , we investigated the ability of synthetic peptides derived from proteins of the Bcl 2 family , namely , the NH 2 terminal region of Bcl 2 ( Bcl2 _ syn ) , a central domain of Bax ( Bax _ syn ) , and a central domain of Bak ( Bak _ syn ) to interfere with the apoptotic process in LLC PK 1 cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Malignant pleural mesothelioma lines and tumors rarely express the antiapoptotic Bcl 2 protein but routinely express the antiapoptotic protein Bcl xl and the proapoptotic proteins Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Our data demonstrated that Gyp induced apoptotic cell death was accompanied by up regulation of Bax , Bak and Bcl 10 ( L ) , and down regulation of Bcl 2 and Bad , while it had no effect on the level of Bag 1 protein . ^^^ Taken together , these results suggest that treatment of human hepatoma cells with Gyp induced apoptosis through the up regulation of Bax and Bak , and down regulation of Bcl 2 , release of mitochondrial cytochrome c and activation of caspase cascade . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunoblotting for Bcl 2 family members revealed no significant changes in the expression levels of Bcl 2 , Bcl 10 ( L ) , Bax or Bak following gene or ' chemogene ' therapy with E2F 1 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Studies with mouse embryo fibroblasts deficient for the BCL 2 family multidomain proapoptotic proteins BAX and BAK have revealed that both of these proteins are essential for apoptosis induced by multiple stimuli , suggesting that these proapoptotic proteins are functionally overlapping in these cells [ M . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Blood and liver were analyzed for plasma aminotransferase activity , liver histology , liver apoptotic nuclei , mRNA of several cytokines ( tumor necrosis factor [ TNF ] alpha , interleukin [ IL ] 1beta , IL 6 , and IL 10 ) , apoptotic ligands ( TRAIL ) , cytokine receptors ( TNFRp 55 ) , pro and antiapoptotic regulators / adaptors ( Fas receptor , FasL , FADD , TRADD , RIP , Bak , Bax , Bcl 10 , Bcl 2 and Bcl w ) , and caspase 8 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We further demonstrated that cytosolic HSP 60 forms a macromolecular complex with bax and bak in vitro suggesting that complex formation with HSP 60 may block the ability of bax and bak to effect apoptosis in vivo . ^^^ To our knowledge , this is the first report suggesting that interactions of HSP 60 with bax and / or bak regulate apoptosis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Pro apoptotic members of the Bcl 2 family can be subdivided in two classes according to their structure : a group including Bax , Bak , and Bok that display Bcl 2 homology ( BH ) 1 , BH 2 and BH 3 domains and a second group including Bid ( BH 3 interacting domain death agonist ) , Bad , Bim ( Bcl 2 interacting mediator of cell death ) and several others that contain only a BH 3 domain , the BH 3 only proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Additionally , Bax and Bak , two pro apoptotic members , seem to be not oligomerized in the mitochondrial membrane following ceramide exposure . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Detailed tissue expression of bcl 2 , bax , bak and bcl 10 in the normal human pancreas and in chronic pancreatitis , ampullary and pancreatic ductal adenocarcinomas . ^^^ METHOD : Expression of bcl 2 , bax , bcl 10 , bak and p 53 was determined in formalin fixed paraffin wax embedded archival specimens of normal pancreatic tissue ( n = 7 ) , chronic pancreatitis ( n = 7 ) , pancreatic ductal adenocarcinoma ( n = 23 ) and ampullary cancer ( n = 7 ) by immunohistochemistry using specific antibodies . ^^^ In pancreatic ductal adenocarcinoma and ampullary cancer , bcl 2 was not detected compared with expression seen in normal acini ( p < 0 . 01 ) , minor ( p < 0 . 001 ) and major ducts ( p < 0 . 01 ) , bax expression was reduced with respect to minor ducts ( p < 0 . 01 ) but no different from normal acini or major ducts . bak and bcl 10 were more strongly expressed in malignant epithelia compared with acini and major ducts but reduced when compared with minor ducts ( p < 0 . 01 ) . ^^^ Differential survival of individual patients was predicted by the relative level of bcl 10 expression but not bax or bak , such that strong expression of bcl 10 was associated with a median postoperative survival of 171 days when compared with 912 days for diminished expression ( p < 0 . 001 ) of bcl 10 . ^^^ CONCLUSION : Pancreatic and ampullary cancer are associated with absent bcl 2 expression . bax , bak and bcl 10 expression was reduced compared with normal minor ducts whilst bak and bcl 10 expression was increased when compared with major ducts . bcl 10 expression correlates with survival following resection and may represent a potential prognosis marker . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Its biological function can be inhibited by proapoptotic proteins such Bak , Bad , and Bax by forming complexes mediated primarily by the Bcl 2 homology 3 ( BH 3 ) domain . ^^^ By using a competition assay , several peptides derived from the BH 3 region of Bak , Bad , Bax , and Bcl 2 were investigated . ^^^ Bad and Bak BH 3 peptides compete efficiently with IC ( 50 ) values of 0 . 048 and 1 . 14 microM , respectively , while the peptides from the BH 3 region of Bcl 2 and Bax compete weakly . ^^^ The relative binding order of the peptides ( Bad > Bak > Bcl 2 > Bax > mutated Bak ) correlates well with previously published results . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The opposite action of anti apoptotic proteins ( Bcl 2 family ) and pro apoptotic proteins ( p 53 , Bax , Bak ) regulates the activation of caspases that are the effectors proteases of the cell suicide . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The active truncated form of BID ( tBID ) triggers the mitochondrial activation of caspase 9 by inducing the activation of BAK or BAX . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We show here that fibroblasts lacking Bak remain susceptible to c Myc induced apoptosis whereas bax deficient fibroblasts are resistant . ^^^ By contrast , there is no synergy between BH 3 peptide and c Myc in fibroblasts deficient in both Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Spontaneous and drug induced apoptosis is mediated by conformational changes of Bax and Bak in B cell chronic lymphocytic leukemia . ^^^ The role of Bax and Bak , 2 proapoptotic proteins of the Bcl 2 family , was analyzed in primary B cell chronic lymphocytic leukemia ( CLL ) cells following in vitro treatment with fludarabine , dexamethasone , or the combination of fludarabine with cyclophosphamide and mitoxantrone ( FCM ) . ^^^ A strong correlation was found between the number of apoptotic cells and the percentage of cells stained with antibodies recognizing conformational changes of Bax ( n = 33 ; r = 0 . 836 ; P < . 001 ) or Bak ( n = 10 ; r = 0 . 948 ; P < . 001 ) . ^^^ Preincubation of CLL cells with Z VAD . fmk ( N benzyloxycarbonyl Val Ala Asp fluoromethyl ketone ) , a broad caspase inhibitor , abolished caspase 3 activation , exposure of phosphatidylserine residues , and reactive oxygen species generation ; partially reversed the loss of transmembrane mitochondrial potential ( DeltaPsim ) ; but did not affect Bax or Bak conformational changes . ^^^ These results indicate that the conformational changes of Bax and Bak occur upstream of caspase activation or are caspase independent . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Activation of Bak , Bax , and BH 3 only proteins in the apoptotic response to doxorubicin . ^^^ Apoptosis correlated with modulation of Bak and Bax to their active conformations . bax as well as bak deficient mouse embryo fibroblasts were resistant to DXR compared with wild type mouse embryo fibroblasts further supporting a role for these proteins as main DXR induced apoptosis regulators . ^^^ Furthermore , using immunocytochemistry as well as chemical blocking of putative apical pathways we could demonstrate that Bak is activated prior to Bax . ^^^ Interestingly , in Bcl 2 transfected cells Bak activation was also blocked , while Bax was still partially active in agreement with differential regulation of these two proteins . ^^^ This enhanced apoptosis was preceded by enhanced Bak and Bax activation , and both responses as well as apoptosis were blocked in transfectants overexpressing Bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The Bcl 2 homology ( BH ) 3 only pro apoptotic Bcl 2 family protein Bim plays an essential role in the mitochondrial pathway of apoptosis through activation of the BH 1 3 multidomain protein Bax or Bak . ^^^ BimEL or Bak BH 3 peptide induces Bax conformational change in vitro only under the presence of mitochondria , and the outer mitochondrial membrane fraction is sufficient for induction of Bax conformational change . ^^^ Interestingly , native Bax is attached loosely on the surface of isolated mitochondria , which undergoes conformational change and insertion into mitochondrial membrane upon stimulation by BimEL , Bak BH 3 peptide , or freeze / thaw damage . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This implicates the mitochondrial apoptotic pathway in this synergy , a notion confirmed by the inability of c Myc to sensitize to RIP killing in cells lacking the obligate mitochondrial apoptotic effectors Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To analyze the mechanisms of the apoptotic activity of Cl F araA , we sought to determine the effects of the drug on the levels of Bcl 2 family proteins ( Bcl 2 , Bcl 10 ( L ) , Mcl 1 , Bax , Bak ) and cell survival signals via Akt . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We have investigated whether subsets of indolent B cell non Hodgkin ' s lymphoma ( IB NHL ) differ in the expression of the bcl 2 family members ; 116 cases of IB NHL , composed of chronic lymphocytic leukemia ( CLL , n = 48 ) , follicular lymphoma ( FL , n = 38 ) , marginal zone B cell lymphoma ( MZBCL , n = 15 ) , and mantle cell lymphoma ( MCL , n = 15 ) , were investigated for expression of bcl 2 , bcl 10 , mcl 1 , bax , and bak proteins by immunohistochemistry . ^^^ The different subsets of IB NHLs differ in their expression of mcl 1 , bax , and bak proteins . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A survey of molecules involved in TRAIL or Bax mediated apoptotic pathways showed no significant change in expression of death receptors , death decoy receptors ; FLIP ; Bcl 2 ; Bcl xS ; Bax ; Bak ; XIAP or caspase 2 , 7 , 8 , or 9 in either DLD1 / Bax R or DLD1 / TRAIL R cells . ^^^ Moreover , DLD1 / Bax R cells were sensitive to adenoviral vectors that expressed the TRAIL gene , but resistant to adenoviral vectors that expressed the Bak gene . ^^^ In contrast , DLD1 / TRAIL R cells were sensitive to adenoviral vectors that expressed either Bax or Bak gene . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The `` BH 3 only ' ' proteins of the BCL 2 family require `` multidomain ' ' proapoptotic members BAX and BAK to release cytochrome c from mitochondria and kill cells . ^^^ We find short peptides representing the alpha helical BH 3 domains of BID or BIM are capable of inducing oligomerization of BAK and BAX to release cytochrome c . ^^^ Another subset characterized by the BH 3 peptides from BAD and BIK can not directly activate BAX , BAK but instead binds antiapoptotic BCL 2 , resulting in the displacement of BID like BH 3 domains that initiate mitochondrial dysfunction . ^^^ These data support a two class model for BH 3 domains : BID like domains that `` activate ' ' BAX , BAK and BAD like domains that `` sensitize ' ' by occupying the pocket of antiapoptotic members . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
BAX and BAK mediate p 53 independent suppression of tumorigenesis . ^^^ BAX and BAK are essential regulators of proapoptotic signaling , and the disruption of apoptosis is linked to the development of cancer . ^^^ To investigate the role of BAX and BAK in tumorigenesis , primary baby mouse kidney epithelial cells ( BMKs ) from wild type , BAX , BAK , or BAK and BAK deficient mice were transformed by adenovirus E1A and dominant negative p 53 ( p53DD ) . ^^^ In contrast , E1A and p53DD transformed BAX and BAK deficient BMKs formed highly invasive carcinomas . ^^^ Transformed BMKs deficient for either BAX or BAK were also tumorigenic , but only when heterozygous for the remaining bax or bak allele , the expression of which was lost in most resulting tumors . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Deficiency in Bak and Bax perturbs thymic selection and lymphoid homeostasis . ^^^ Bak and Bax are required and redundant regulators of an intrinsic mitochondrial cell death pathway . ^^^ To analyze this pathway in T cell development and homeostasis , we reconstituted mice with Bak ( / ) Bax < ( / ) hematopoietic cells . ^^^ We found that the development and selection of Bak ( / ) Bax ( / ) thymocytes was disrupted , with altered representation of thymic subsets and resistance to both death by neglect and antigen receptor induced apoptosis . ^^^ Elimination of Bak ( / ) Bax ( / ) T cells that responded to endogenous superantigen was also reduced . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Although protein expression of Fas , FADD , Bax , Bak , and Bcl 10 in the whole cell lysates was not changed by H pylori , Bax was decreased from mitochondria free cytosol suggesting that Bax was translocated into mitochondria . ( 3 ) Cell death and the activities of caspases 3 and 8 were promoted in MKN 45 cells stably expressing super repressor IkappaBalpha that inhibits NFkappaB activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The Bcl 2 , Mcl 1 , Bcl xL / S , Bcl w , Bax , Bak , and Bad were shown to be expressed in both malignant and non neoplastic , normal plasma cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Pro apoptotic Bcl 2 family members such as bax or bak are clearly required to initiate cytochrome c / apaf 1 / caspase 9 mediated cell death during oxygen deprivation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We also detected the expression of Bax , Bak , p 53 , Bcl 2 , Bcl 10 ( L ) , AIF and MRP 1 by Western blots . ^^^ Bcl 2 protein expression was significantly increased in p 50 , p 46 and p 33 transfected cells , while the expression of Bax , Bak , p 53 , Bcl 10 ( L ) and MRP 1 was essentially unchanged . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Recent genetic studies with fibroblasts derived from mutant mouse embryos indicate that a class of the BCL 2 family proapoptotic proteins ( designated BH 123 or multidomain proteins ) such as BAX and BAK constitutes an essential component of the core apoptosis machinery in animal cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We hypothesized that apoptosis is a downstream event in erectile dysfunction , and pro apoptotic ( Bak and Bax ) and anti apoptotic ( Bcl 2 and Bcl 10 ) factors are involved in the etiology of aging erectile dysfunction . ^^^ Gene expression of pro apoptotic ( Bak and Bax ) and anti apoptotic ( Bcl 2 and Bcl 10 ) factors were then analyzed by reverse transcription polymerase chain reaction . ^^^ Gene and protein expression of the pro apoptotic genes Bak and Bax was detected in the crura of all age groups but there was no significant difference in young and old rat crura . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Semiquantitative RT PCR and Western blotting revealed activation of cell death related genes Bak and Bax of the Bcl 2 family . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Pro apoptotic members possessing BH 1 , BH 2 , and BH 3 domains ( such as Bax and Bak ) act as a gateway for a variety of apoptotic signals . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The release of cytochrome c is the central gate in turning on / off apoptosis , and is regulated by the interaction of proapoptotic proteins , including Bid , Bax and Bak , and antiapoptotic proteins including Bcl 2 and Bcl 10 ( L ) , and a specific class of inhibitors of apoptosis proteins ( IAPs ) including Akt , survivin , and heat shock proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Association of Bax and Bak homo oligomers in mitochondria . ^^^ Bax requirement for Bak reorganization and cytochrome c release . ^^^ Here we report that following Bax translocation in ATP depleted rat proximal tubule cells , Bak , a proapoptotic molecule that normally resides in mitochondria , also reorganizes to form homo oligomers . ^^^ Oligomerization of both Bax and Bak occurred independently of Bid cleavage and / or translocation . ^^^ Western blots of chemically cross linked membrane extracts showed nonoverlapping `` ladders ' ' of Bax and Bak complexes in multiples of approximately 21 and approximately 23 kDa , respectively , consistent with molecular homogeneity within each ladder . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The Bcl 2 homology 3 ( BH 3 ) domain is present in most members of the Bcl 2 protein family and is required to confer the death inducing properties of pro apoptotic members , including Bax , Bak , Bad , and Bik , in cell based assay systems . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 members can either be anti ( Bcl 2 , Bcl 10 ( L ) , Bcl w ) or pro apoptotic ( Bax , Bak , Bid , Bad , Bcl 10 ( S ) ) . ^^^ The expression of the pro apoptotic members Bax , Bak , Bid , and Bcl 10 ( S ) was significantly ( P < 0 . 05 ) decreased after TPN . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of anti apoptotic proteins ( Bcl 2 , Bcl 10 ( L ) ) and pro apoptotic proteins ( Bax , Bcl 10 ( S ) , Bad , and Bak ) in response to cryo injury varied in this cell line panel . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Using cultured prostate cancer ( PC ) cell lines , LN CaP and ALVA 31 , we studied the effects of 1alpha , 25 ( OH ) 2 Vitamin D 3 ( VD 3 ) on expression of several apoptosis regulating proteins including : ( a ) Bcl 2 family proteins ( Bcl 2 , Bcl 10 ( L ) , Mcl 1 , Bax , and Bak ) ; ( b ) the heat shock protein 70 binding protein BAG1L ; and ( c ) IAP family proteins ( XIAP , cIAP 1 , and cIAP 2 ) . ^^^ VD 3 induced decreases in levels of antiapoptotic proteins Bcl 2 , Bcl 10 ( L ) , and Mcl 1 , BAG1L , XIAP , cIAP 1 , and cIAP 2 ( without altering proapoptotic Bax and Bak ) in association with increases in apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Two pathways for tBID induced cytochrome c release from rat brain mitochondria : BAK versus BAX dependence . ^^^ Immunoblotting showed the presence of BAK , but not BAX , in brain mitochondria . tBID did not release Cyt c from rat liver mitochondria , which lacked both BAX and BAK . ^^^ This indicated that tBID did not act independently of BAX and BAK . tBID plus monomeric BAX produced twice as much Cyt c release as did tBID or oligomeric BAX alone . ^^^ Koenig ' s polyanion , an inhibitor of VDAC , suppressed tBID induced Cyt c release from brain mitochondria mediated by BAK but not by BAX . ^^^ Thus , tBID can induce mPT independent Cyt c release from brain mitochondria by interacting with exogenous BAX and / or with endogenous BAK that may involve VDAC . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In human KB epithelial cells expressing the caspase resistant mutant crBAP 31 , Fas stimulation resulted in cleavage of BID and insertion of BAX into mitochondrial membrane , but subsequent oligomerization of BAX and BAK , egress of cytochrome c to the cytosol , and apoptosis were impaired . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This increased apoptosis was accompanied by decreased antiapoptotic bcl 2 mRNA expression among bcl 2 related genes ( bcl 2 , bax , bak , mcl 1 , and bcl 10 ( L / S ) ) , and the effect was also more prominent in the cagA ( + ) strains . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The results demonstrated a tendency for stronger and more frequent expressions of c myc , Bak and Bax despite a rather weaker expression of Bcl 2 in cancer tissues from the elderly compared with those from the younger patients . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Nonetheless , there were no significant alterations in the level of Bcl 2 , Bcl 10 ( L ) , Bax and Bak by the proteasome inhibitor , nor any evidence of cytochrome ( cyt ) c release into cytosol from dying cells , suggesting that cyt c is not involved . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bak expression was compared with our previous investigated apoptosis related parameters such as apoptotic index ( AI ) , Bax and Bcl 2 expression , and p 53 accumulation . ^^^ No significant correlation was found between Bak expression and Bax expression , AI , or p 53 accumulation . ^^^ A two parameter combination of Bak expression and Bax expression , AI , or p 53 accumulation revealed an enhanced prognostic potential ( p < 0 . 0001 ) when compared with single parameters . ^^^ We conclude that Bak expression , particularly in combination with Bax expression , as well as in combination with AI , or p 53 accumulation , has prognostic value in tongue SCC . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Inhibition of Bid induced apoptosis by Bcl 2 . tBid insertion , Bax translocation , and Bax / Bak oligomerization suppressed . ^^^ Bid , Bax , and Bak ) or anti apoptotic ( e . g . ^^^ Finally , Bcl 2 diminished Bid induced oligomerization of Bax and Bak within the membrane bound organellar fraction , shown by cross linking experiments . ^^^ Critical steps blocked by Bcl 2 included tBid insertion , Bax translocation , and Bax / Bak oligomerization in the mitochondrial membranes . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunoblotting revealed that the protein profiles of Bax , Bak and Bad were different during the progression of neuronal apoptosis in the LGN . ^^^ Bax underwent a subcellular redistribution by 1 day post lesion , while Bak increased later . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
They interact with the anti apoptotic Bcl 2 family members and induce apoptosis by a mechanism that requires the presence of at least one of the multidomain pro apoptotic proteins Bax or Bak . ^^^ Although the BH 3 domain of Bid can promote the pro apoptotic assembly and function of Bax / Bak by itself , other BH 3 domains do not function as such . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A similar result was obtained upon the substitution of glycine 145 with alanine in the BH 1 domain ( Bcl 2 / G145A ) , which failed to interact with either Bax or Bak . ^^^ Pro apoptotic Bax and Bak have been known to be activated in response to antitumor drugs , and Bcl 2 / G145A as well as Bcl 2 / DeltaBH1 also accelerated Bax or Bak induced apoptosis in HEK293T cells . ^^^ These two mutants still retained the ability to interact with wild type Bcl 2 and Bcl xL , and abrogated the inhibitory effect of wild type Bcl 2 or Bcl xL on Bax or Bak induced apoptosis . ^^^ In addition , immunoprecipitation studies revealed that Bcl 2 / DeltaBH1 and Bcl 2 / G145A interrupted the association between wild type Bcl 2 and Bax / Bak . ^^^ Taken together , our results demonstrate that Bcl 2 / DeltaBH1 or Bcl 2 / G145A acts as a dominant negative of endogenous anti apoptotic proteins such as Bcl 2 and Bcl xL , thereby enhancing antitumor drug induced apoptosis , and that this dominant negative activity requires both a failure of interaction with Bax and Bak through the BH 1 domain of Bcl 2 and retention of the ability to interact with Bcl 2 and Bcl xL . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The activation of caspases after brain ischaemia is largely consequent on the translocation of Bax , Bak , and other BH 3 only members of the Bcl 2 family to the mitochondrial outer membrane and the release of cytochrome c , procaspase 9 , and apoptosis activating factor 1 ( Apaf 1 ) from the mitochondrial intermembrane space . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Involvement of proapoptotic molecules Bax and Bak in tumor necrosis factor related apoptosis inducing ligand ( TRAIL ) induced mitochondrial disruption and apoptosis : differential regulation of cytochrome c and Smac / DIABLO release . ^^^ Activation of BID , a `` BH 3 domain only ' ' Bcl 2 family member , triggers the oligomerization of proapoptotic family members Bak or Bax , resulting in the release of mitochondrial proteins to cytosol . ^^^ In this study , we have shown the importance of Bax and Bak in TRAIL induced apoptosis by studying in murine embryonic fibroblasts ( MEFs ) from Bax ( / ) and Bak ( / ) animals . ^^^ TRAIL induced cytochrome c release and apoptosis in wild type , Bid ( / ) , Bax ( / ) , or Bak ( / ) MEFs , but not in Bax ( / ) Bak ( / ) double knockout ( DKO ) MEFs . ^^^ Unlike cytochrome c release , TRAIL induced Smac / DIABLO release was blocked in Bid ( / ) , Bax ( / ) , Bak ( / ) , or DKO MEFs , suggesting the differential regulation of these mitochondrial proteins during apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To investigate whether the Bcl 2 gene family is involved in modulating mechanism of apoptosis and change of cell cycle protein induced by curcumin in acute myeloid leukemia HL 60 cell line and primary acute myelogenous leukemic cells , the Bcl 2 family member Mcl 1 , Bax and Bak and cell cycle proteins including P27kipl , P21wafl , cyclin D 3 and pRbp were selected and their expression detected by SABC immuno histochemical stain method . ^^^ It was found that when HL 60 cells were treated with 25 mumol / L curcumin for 24 h , the expression level of Mcl 1 was down regulated , but that of Bax and Bak up regulated time dependently . ^^^ There was significant difference in the expression level of Mcl 1 , Bax and Bak between the curcumin treated groups and control group ( P < 0 . 05 0 . 01 ) . ^^^ At the same time , curcumin had no effect on progress of cell cycle in primaty acute myelogenous leukemia at newly diagnosis , but could increase the peak of Sub G 1 ( P < 0 . 05 ) , and down regulate the expression of Mcl 1 and up regulate the expression of Bax and Bak with the difference being statistically significant . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
BAX and BAK regulation of endoplasmic reticulum Ca2+ : a control point for apoptosis . ^^^ BAX and BAK are `` multidomain ' ' proapoptotic proteins that initiate mitochondrial dysfunction but also localize to the endoplasmic reticulum ( ER ) . ^^^ Mouse embryonic fibroblasts deficient for BAX and BAK ( DKO cells ) were found to have a reduced resting concentration of calcium in the ER ( [ Ca2+ ] er ) that results in decreased uptake of Ca2+ by mitochondria after Ca2+ release from the ER . ^^^ A third set of stimuli , including many intrinsic signals , required both ER released Ca2+ and the presence of mitochondrial BAX or BAK to fully restore apoptosis . ^^^ Thus , BAX and BAK operate in both the ER and mitochondria as an essential gateway for selected apoptotic signals . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
BH 3 ( Bcl 2 homology 3 ) only proteins of the Bcl 2 family activate Bax or Bak during apoptosis to promote the release of pro death factors sequestered in the mitochondrial intermembrane space . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Calcitriol induced cell death was regulated by members of the Bcl 2 family of apoptosis regulatory proteins , as shown by calcitriol induced up regulation of proapoptotic Bax and Bak and the lack of calcitriol induced cytotoxicity in Bcl 2 overexpressing insulinoma cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Using Western blots to compare protein levels with those of HEC not treated with 5 fluorouracil , the fold changes in HEC 18 and HEC 18T in LDL free medium were 1 . 6 6 . 1 fold lower for pro apoptotic p 53 , Bak and Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
They communicate this information to the pro apoptotic ' multidomain ' members Bax or Bak a process that is antagonized by anti apoptotic members of the Bcl 2 family . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Caspase 8 cleaves BID to tBID , which targets mitochondria and induces oligomerization of BAX and BAK within the outer membrane , resulting in release of cytochrome c from the organelle . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
BH 3 only molecules induce the activation of the multidomain proapoptotics BAX and BAK , resulting in the permeabilization of the outer mitochondrial membrane and the efflux of cytochrome c . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Mitochondrial membrane permeabilisation by Bax / Bak . ^^^ Recent studies on cells derived from mice deficient in both multi domain pro apoptotic genes of the Bcl 2 family , Bax and Bak , suggest that one or other of these proteins are required for the release of apoptogens such as cytochrome c from mitochondria . ^^^ In addition BH 3 only proteins of this family such as Bid are suggested to act as critical death inducing ligands via interactions with pro and anti apoptotic Bcl 2 family proteins with Bax or Bak at the mitochondrial surface . ^^^ Despite this increase in knowledge it remains unclear precisely how Bak and Bax promote outer mitochondrial membrane ( OMM ) permeabilisation . ^^^ We suggest that Bax and Bak may not operate in precisely the same manner and evaluate the current models for their function . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Both CPX and NFX * cause Bax and Bak to adopt their apoptotic conformation and to insert into mitochondrial membranes . ^^^ Bax / Bak / double knockout cells fail to undergo MMP and cell death in response to CPX or NFX induced LMP . ^^^ The single knockout of Bax or Bak ( but not Bid ) or the transfection enforced expression of mitochondrion targeted ( but not endoplasmic reticulum targeted ) Bcl 2 conferred protection against CPX ( but not NFX * ) induced MMP and death . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The objective was to evaluate the immunohistochemical expression of p 53 , p 21 , bax , bak , fas , bcl 2 and bcl 10 proteins in 10 endometriomas , 20 benign ovarian tumours ( 10 mucinous , 10 serous ) and 30 malignant ovarian tumours ( 9 mucinous , 19 serous ; 2 endometrioids ) . p 53 positive cells ( mean+ / SD ) in endometriomas , and benign and malignant tumours were 1 . 9+ / 3 . 2 , 0 and 16 . 2+ / 33 . 0 , respectively . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Zinc inhibits Bax and Bak activation and cytochrome c release induced by chemical inducers of apoptosis but not by death receptor initiated pathways . ^^^ In response to activation of the chemical mediated death pathway by anisomycin , 0 . 3 mM zinc inhibited Bax and Bak activation , cytochrome c release , and all of the subsequent steps in apoptosis . ^^^ In the receptor mediated death pathway initiated by Fas or tumor necrosis factor , 3 mM zinc was required to inhibit apoptosis as judged by inhibition of caspase 3 activity and DNA digestion , but it failed to inhibit cytochrome c release , activation of Bax and Bak , or upstream signaling events in this pathway . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
It was revealed that LIGHT treatment resulted in down regulation of anti apoptosis Bcl 2 family member : Bcl 2 , Bcl 10 ( L ) , Bag 1 , and Mcl 1 ; up regulation of pro apoptosis Bcl 2 family member : Bak and Ser ( 112 ) phosphor Bad ; down regulation of pro apoptosis Bcl 2 member Bax ; the other pro apoptosis member Bid remains unaltered . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
As for ' multidomain ' pro apoptotic members ( Bax , Bad and Bok / Mtd ) , Bax and Bak are highly expressed throughout differentiation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Apoptosis was induced by sodium nitroprusside ( SNP ) dihydrate , which generates NO , or by staurosporine , which is a proapoptotic agent dependent upon Bax or Bak protein . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We also analyzed the relationship between TCF 4 gene splicing isoforms , proliferation ( proliferating cell nuclear antigen labeling index ) , and apoptosis [ antiapoptotic factors ( Bcl 2 and Bcl 10 ( L ) ) , proapoptotic factors ( Bak and Bax ) , and caspase 3 ] in RCC samples . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
PURPOSE : We hypothesized that apoptosis is a downstream event in erectile dysfunction , and pro apoptotic ( Bak and Bax ) and anti apoptotic ( Bcl 2 and Bcl 10 ) factors are involved in the etiology of diabetes induced erectile dysfunction . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
C terminally truncated Bax , a structural analogue of N Bak , was also neuroprotective , whereas Blk , a different BH 3 only protein was apoptotic in neurons . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
During the process , the expression of COX 2 mRNA and protein and Bcl 2 protein was down regulated , while that of Bax and Bak proteins was up regulated , and the activity of caspase 3 was elevated . ^^^ CONCLUSION : TGZ inhibits cell proliferation and induces apoptosis in HepG 2 cells , which may be associated with the activation of caspase 3 like proteases , down regulation of the expression of COX 2 mRNA and protein , Bcl 2 protein , the elevation of PGE 2 levels , and up regulation of the expressions of Bax and Bak proteins . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Nonredundant role of Bax and Bak in Bid mediated apoptosis . ^^^ Animal models suggest that Bax and Bak play an essential role in the implementation of apoptosis and as a result can hinder tumorigenesis . ^^^ We found that all the tumors expressed Bak , while three did not express Bax . ^^^ Bax / Bak single or double deficiency had no influence on either the clonogenicity or the growth of tumors in Swiss nude mice . ^^^ Cells lacking both Bax and Bak ( i . e . , Bak ( ) BdGBM ) were completely resistant to all stimuli including the microinjection of C 8 and GrB . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Mouse embryonic fibroblasts lacking the expression of both Bax and Bak are resistant against hydroxychloroquine induced apoptosis . ^^^ Such Bax ( / ) Bak ( / ) cells manifest normal LMP , yet fail to undergo MMP and subsequent cell death . ^^^ The data reported herein indicate that LMP does not suffice to trigger caspase activation and that Bax / Bak dependent MMP is a critical step of LMP induced cell death . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis . ^^^ Bax and Bak play a redundant but essential role in apoptosis initiated by the mitochondrial release of apoptogenic factors . ^^^ In addition to their presence at the mitochondrial outer membrane , Bax and Bak can also localize to the ER . ^^^ In wild type cells , this is associated with caspase 12 cleavage that is abolished in bax / bak / cells . ^^^ In bax / bak / cells , introduction of Bak mutants selectively targeted to either mitochondria or the ER can induce apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Interestingly , Nbk failed to induce apoptosis in the absence of Bax , even despite expression of the related molecule Bak . ^^^ Since , in addition , Nbk did not localize to the mitochondria , our data suggest a model in which Nbk acts as an indirect killer to trigger Bax dependent apoptosis , whereas Bak is not sufficient to confer sensitivity to Nbk . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
RT PCR and RNase protection also showed that key pro apoptotic factors including bax , bad and bak do not change in expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
METHODS : Serial tissue sections from paraffin embedded needle biopsy specimens obtained at approximately 1 hr of reperfusion after transplantation of 13 CAD and 12 living related donor ( LRD ) renal allografts were examined by using the terminal deoxynucleotide transferase mediated dUTP nick end labeling assay to detect apoptosis and by immunohistochemistry for expression of key pro apoptotic molecules ( Bax , Bak , tumor necrosis factor receptor [ TNFR ] 1 , Fas , and cytochrome c ) . ^^^ Bax was expressed in 100 % of CAD versus 17 % of LRD renal allografts ( P < 0 . 001 ) , Bak in 92 % of CAD versus 17 % of LRD renal allografts ( P < 0 . 001 ) , and TNFR 1 in 100 % of CAD versus 58 % of LRD renal allografts ( P < 0 . 05 ) . ^^^ Bax and Bak were expressed predominantly in apoptotic cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Interferon alpha induced apoptosis in U 266 cells is associated with activation of the proapoptotic Bcl 2 family members Bak and Bax . ^^^ Here , we show that both proapoptotic Bcl 2 family members Bak and Bax were activated by IFNalpha , strictly in correlation with the induction of apoptosis . ^^^ Using double stainings , we demonstrated that Bak was activated prior to cytochrome c ( cyt c ) release and caspase 3 activation , whereas activated Bax was only found in cells with released cyt c , mitochondrial depolarization , as well as activated caspase 3 . ^^^ Furthermore , IFNalpha induced activation of Bak , and to a large extent also of Bax , was dependent on caspase activity . ^^^ Overexpression of Bcl 2 blocked apoptosis induced by IFNalpha totally abolished Bak activation , as well as decreased the amount of activated Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Proapoptotic bcl 2 family members , Bax and Bak , are essential for developmental photoreceptor apoptosis . ^^^ The purpose of this study was to characterize the roles in retinal development of the proapoptotic Bcl 2 family members Bax and Bak . ^^^ METHODS : Eyes from mice at postnatal day ( P ) 7 , during the peak of developmental apoptosis in the retina , were processed for TdT dUTP terminal nick end labeling ( TUNEL ) to determine whether Bax knockout or double Bax / Bak knockout causes a defect in developmental apoptosis . ^^^ Adult ( > 2 month old ) eyes from wild type , Bak ( / ) , Bax ( / ) , and Bax ( / ) Bak ( / ) mice were analyzed by histology and immunocytochemistry to identify persistent retinal cells . ^^^ RESULTS : Adult Bax ( / ) Bak ( / ) eyes showed significant increases in the number of inner retinal cells , with an almost complete absence of TUNEL positive cell death at P 7 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Pro apoptotic activity of transiently expressed BCL 2 occurs independent of BAX and BAK . ^^^ The pro apoptotic activity of BCL 2 is also observed in a Bax null cells in which BAK expression is inhibited by stable RNAi expression . ^^^ Our results suggest that BCL 2 contains an intrinsic pro apoptotic activity and can induce apoptosis independent of BAX and BAK under specific conditions . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To further understand such merosin driven survival signaling , we analyzed the expression of five Bcl 2 homologs ( Bcl 2 , Bcl 10 ( L ) , Bax , Bak , Bad ) and one non homologous associated molecule ( Bag 1 ) in normal and merosin deficient myotubes , with or without pharmacological inhibitors for Fyn and p 38 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Caspase activation is associated with accumulation of the pro apoptotic proteins Bax and Bak that undergo conformational changes and relocalization to the mitochondria . ^^^ Transient transfection of either a dominant negative mutant of FADD , E 8 , or MC 159 viral proteins that interfere with the DISC function , decreases the apoptotic response of SW 480 cells to resveratrol and partially prevents resveratrol induced Bax and Bak conformational changes . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
LPS stimulation induced the expression of Fas , caspase 8 , cellular FLIP Bfl 1 / A1 , and Bcl 10 , but not FasL , TNFR p 55 , Bak , Bax , and Bad at the transcriptional level . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
PS 341 treatment by itself does not affect the levels of Bax , Bak , caspases 3 and 8 , c Flip or FADD , but elevates levels of TRAIL receptors DR 4 and DR 5 . ^^^ Similarly , murine embryonic fibroblasts lacking Bax undergo apoptosis when exposed to the combination of PS 341 and TRAIL ; however , fibroblasts lacking Bak are significantly resistant . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
However , whereas combination treatment applied to in vitro cell culture was characterized by a significant up regulation and activation of Bax and down regulation of Bcl xL , the treatment applied to tumors induced Bak and Bcl xS , whereas Bcl omega and Bcl xL were down regulated . ^^^ Because there are multiple members of the Bcl 2 family ( 24 members to date ) , these data indicate that , under different biological conditions , different proteins may be responsible for activating apoptosis and provide evidence for a differential regulation of the multidomain Bcl 2 protein encoding genes , bax and bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Our previous results showed that Bcl B binds Bax and suppresses apoptosis induced by over expression of Bax ; however , Bcl B does not bind or suppress Bak . ^^^ To explore the molecular basis for the differential binding and suppression of Bax and Bak , we studied the BH 3 dimerization domains of Bax and Bak . ^^^ Chimeric mutants of Bax and Bak were generated that swapped the BH 3 domains of these pro apoptotic proteins . ^^^ Bcl B associated with and blocked apoptosis induced by mutant Bak containing the BH 3 domain of Bax , but not mutant Bax containing the BH 3 domain of Bak . ^^^ In contrast , Bcl 10 ( L ) protein bound and suppressed apoptosis induction by Bax , Bak and both BH 3 domain chimeras . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Moreover , although reactive oxygen species ( ROS ) overproduction appears to be instrumental for 4 HPR induced MMP and apoptosis , inhibition of the NF kappaB or p 53 mediated signal transduction pathways failed to modulate 4 HPR induced apoptosis . 4 HPR was found to cause an antioxidant inhibitable conformational change of both Bax and Bak , leading to the exposure of their N termini and to the mitochondrial relocalization of Bax . ^^^ Cells with a Bax ( / ) Bak ( / ) genotype were resistant against the 4 HPR induced MMP , overproduction of ROS and cell death . ^^^ Altogether , these data indicate that 4 HPR induces MMP through an ROS mediated pathway that involves the obligatory contribution of the proapopotic Bcl 2 family members Bax and / or Bak . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
After antigen driven expansion , the majority of T cells involved in an immune response die rapidly by apoptosis dependent on the Bcl 2 related proteins , Bim and Bax or Bak . ^^^ Our results suggest a way in which both Bim and Bax / Bak might be required for activated T cell apoptosis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , in contrast to the anti apoptotic Bcl 2 proteins , BHRF 1 does not bind tightly to peptides derived from the pro apoptotic proteins Bak , Bax , Bik , and Bad . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In the sensitive SCLC cell line , IR induced conformational modulation of Bak and Bax , mitochondrial depolarization , and nuclear fragmentation . ^^^ However , in the same cells , cisplatin , a DNA damaging drug , induced Bak and Bax modulation , mitochondrial depolarization , and nuclear fragmentation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Analysis of the expression of the members of the Bcl 2 family indicated that the synthetic glucocorticoid increased Bax protein levels without affecting the levels of Bcl 2 , Bcl XL , Bcl XS , or Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
These events were associated with Bcl 2 cleavage , Bax , Bak , and Bad accumulation , mitochondrial translocation of Bax , abrogation of Mcl 1 , Bcl xL , and XIAP upregulation , and a marked induction of JNK and p 53 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A Bax / Bak independent mitochondrial death pathway triggered by Drosophila Grim GH 3 domain in mammalian cells . ^^^ These Grim GH 3 activities do not require Bax or Bak function , revealing GH 3 activity as the first proapoptotic stimulus able to trigger the mitochondrial death pathway in mammalian cells in the absence of multidomain proapoptotic Bcl 2 proteins . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The antiapoptotic protein BCL 2 prevents this mitochondrial loop , while the `` multidomain ' ' proapoptotic proteins BAX and BAK are crucial to initiate it . ^^^ BCL 2 , BAX and BAK localize also to the endoplasmic reticulum ( ER ) , the main intracellular Ca ( 2+ ) store . ^^^ Cells deficient for Bax , Bak ( DKO ) display lowered steady state ER Ca ( 2+ ) concentrations ( [ Ca ( 2+ ) ] ( er ) ) and secondarily decreased mitochondrial Ca ( 2+ ) uptake . ^^^ Thus , BAX and BAK control apoptosis not only at the mitochondria , but also at the ER , an obligate checkpoint for Ca ( 2+ ) dependent apoptotic stimuli . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
SBHA appeared to sensitize melanoma to TRAIL induced apoptosis by up regulation of pro apoptotic proteins in the TRAIL induced apoptotic pathway such as caspase 8 , caspase 3 , Bid , Bak , and Bax , and up regulation of the BH 3 domain only protein , Bim . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Moreover , despite butyrate mediated translocation of proapoptotic Bax and Bak to the mitochondria , fewer cells with elevated intrinsic Deltapsi ( m ) exhibit concomitant cytochrome c release , and cells with elevated Deltapsi ( m ) undergo significantly lower levels of Deltapsi ( m ) dissipation and apoptosis than parental cells , or cells with decreased Deltapsi ( m ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The molecular mechanism ( s ) of IRF 5 mediated growth inhibition is associated with a G ( 2 ) M cell cycle arrest and modulation of growth regulatory and proapoptotic genes , including p 21 , Bak , DAP kinase 2 , and Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
These responses would be expected to activate the pro apoptotic multi BCL homology domain proteins BAX and BAK , leading to the previously reported release of cytochrome c observed during oxysterol induced apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
CD4+ T cells from SIVmac 251 infected macaques showed upregulation of the death ligand ( CD95L ) and of the proapoptotic proteins Bim and Bak , but not of Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In IEC 6 cells treated with either IL 15 or KM12SM conditioned medium , immunoblotting revealed a decrease in the production of p21Waf1 , Bax , and Bak and an increase in the production of cyclin E , proliferating cell nuclear antigen , the phosphorylated active form of AKT , basic fibroblast growth factor , and vascular endothelial growth factor , changes associated with cell growth , survival , and induction of angiogenesis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Antiapoptotic family proteins such as Bcl 2 and Bcl 10 ( L ) function , at least in part , by binding proapoptotic members such as Bax and Bak and thereby preventing release of apoptotic proteins , including cytochrome c , from the mitochondria . `` BH 3 only ' ' members of the family disrupt this interaction by binding , via their BH 3 domain , to a hydrophobic pocket on the surface of the antiapoptotic members . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In this study , we found that NPCs deficient in Apaf 1 , or both the pro apoptotic multidomain Bcl 2 family members Bax and Bak , were resistant to cytosine arabinoside and gamma irradiation induced apoptosis . ^^^ Conversely , DNA damage induced reactive oxygen species generation was inhibited significantly by gene disruption of p 53 , Apaf 1 , or caspase 9 , and combined deficiency of Bax and Bak , but not by caspase 3 or caspase 6 deficiency . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To investigate the mechanisms responsible for survival and apoptosis / anoikis in normal human intestinal epithelial crypt cells , we analyzed the roles of various signaling pathways and cell adhesion on the expression of six Bcl 2 homologs ( Bcl 2 , Bcl XL , Mcl 1 , Bax , Bak , Bad ) in the well established HIEC 6 cell model . ^^^ For example , the inhibition of the PI 3 K / Akt 1 pathway down regulated Bcl XL , Mcl 1 , and Bad , while at the same time up regulating Bax , whereas the inhibition of Fak up regulated both Bax and Bak , down regulated Bad , and did not affect the other Bcl 2 homologs analyzed . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This family of proteins now includes both anti apoptotic molecules such as Bcl 2 and Bcl 10 ( L ) , and pro apoptotic molecules such as Bax , Bak , Bid , and Bad . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Myc sensitization to oxygen deprivation induced cell death is dependent on Bax / Bak , but is independent of p 53 and hypoxia inducible factor 1 . ^^^ Our results demonstrate that murine embryonic fibroblasts from bax / bak / mice that conditionally express c Myc did not die in response to either oxygen or serum deprivation . ^^^ Thus , oxygen deprivation induced cell death in fibroblasts with deregulated expression of c Myc is independent of p 53 or HIF 1 status , but is dependent on the Bcl 2 family member Bax or Bak to initiate mitochondrial dependent cell death . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In hypoxic renal cells , Bax and Bak , 2 pro apoptotic proteins of the Bcl 2 family , collaborate to permeabilize the mitochondrial outer membrane to intermembrane proteins such as Cyt c , although Bax , per se , appears to play the dominant role . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Ether lipid resistant S49ar cells were cross resistant to extracellular stress factors ( cold shock , heat shock , H2O2 , dimethylsulfoxide ) and to radiation induced apoptosis but not to physiological apoptotic signals ( dexamethasone , growth factor deprivation , thapsigargin , C 2 ceramide ) and expressed similar levels of the apoptosis regulating proteins Bcl 2 , Bcl 10 , Bax , Bad and Bak as did the parent S49wt cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Central to the regulation of the mitochondrial checkpoint is a complex three way interplay between members of the BCL 2 family , which are comprised of an antiapoptotic subgroup including BCL 2 itself , and the proapoptotic BAX , BAK and BH 3 domain only subgroups . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast to Bax / cells , Bak deficient human cancers undergo apoptosis in response to TRAIL or CPT 11 , implying that these proteins have nonoverlapping functions . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The proapoptotic activities of Bax and Bak limit the size of the neural stem cell pool . ^^^ The proapoptotic Bcl 2 family members Bak and Bax play central and redundant roles in the regulation of apoptosis . ^^^ In this study , we investigated the effect of loss of Bax and Bak in the CNS . ^^^ The adult bax / bak / mice display masses of densely staining cells in the proliferative zones of the brain . ^^^ Both neural progenitor cells and mature neurons derived from bax / bak / mice were resistant to various apoptotic stimuli . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The aim of this study was to evaluate odontogenic myxomas for the expression of cell cycle protein Ki 67 , apoptosis regulating proteins Bcl 2 , Bcl XL , Bak , and Bax , and matrix metalloproteinases MMP 2 , MMP 3 , and MMP 9 . ^^^ Twenty six paraffin embedded tissue sections were used in a standard immunohistochemistry protocol and incubated with one of the following antibodies : Bcl 2 , Bcl XL , Bak , Bax , or Ki 67 . ^^^ Proapoptotic proteins ( Bak and Bax ) were not detected in tumor cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We found that Ad / p53 induced the expression of the proapoptotic genes PUMA , Bak , Bax , and Fas in a cell type and time dependent manner . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Akt also antagonized tBID mediated BAX activation and mitochondrial BAK oligomerization , two downstream events thought to be critical for tBID induced apoptosis . ^^^ These results suggest that Akt inhibits BID mediated apoptosis downstream of BID cleavage via promotion of mitochondrial hexokinase association and antagonism of tBID mediated BAX and BAK activation at the mitochondria . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
METHODS : We performed semi quantitative RT PCR to examine the expression level of bak , bax , bcl 2 and bcl xL in 70 % hepatectomized rat livers during the whole regeneration process and compared to that of the sham and normal groups . ^^^ RESULTS : The expression of bak and bax was decreased whereas that of bcl 2 and bcl xL was increased in hepatectomized animals compared to normal liver at most time points . ^^^ We also reported for the first time that sham group of animals had statistically significant higher expression of bak and bax than hepatectomized animals . ^^^ CONCLUSION : The expression changes of bak , bax , bcl 2 and bcl xL genes are altered not only due to regeneration , but also due to effects of surgical operations . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
G110R substitution confers on Bcl 2 ( 1 ) substantially increased binding affinity to Bak , Bad and Bax BH 3 peptides , demonstrating that R 110 is a key contributor to the BH 3 binding affinity of Bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Decreases in cellular metabolism may sensitize cells to activation and action of the pro apoptotic Bcl 2 family members , Bak and Bax , and promote apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The reduction of interstitial fibrosis is accompanied by an increase in myocardial hHO 1 expression in peri infarct border areas , concomitant with higher Bcl 2 levels and lower Bax , Bak , and caspase 3 levels in the ischemic myocardium compared with saline control . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The ability of RB + AR to induce mitochondria damage was dependent on the proapoptotic proteins Bax and Bak and could be blocked by the antiapoptotic protein Bcl 10 ( L ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of the proapoptotic protein Bak was increased and Bax cleavage and conformational change was observed in Roscovitine treated B CLL cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Using RNA protection assays we found constitutive expression of most bcl 2 members with high levels of bcl 2 , bcl w , bad , bak , bax , and the bcl 2 / bax ratio , compared to normal PBL . ^^^ Spontaneous apoptosis of B CLL cells by in vitro culture resulted in decreased bcl 2 , bcl w , bfl 1 , mcl 1 , bak , bax , and bcl 2 / bax expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Pro apoptotic proteins of the Bcl 2 family , Bax and Bak , exhibited conformational changes in neural precursors expanding in vitro . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Macroarrays led to the identification of several Env elicited , p 53 dependent proapoptotic transcripts , in particular Puma , a proapoptotic `` BH 3 only ' ' protein from the Bcl 2 family known to activate Bax / Bak . ^^^ Down modulation of Puma by antisense oligonucleotides , as well as RNA interference of Bax and Bak , prevented Env induced apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Here we examine the distribution and role death repressors bcl 2 , bcl 10 ( L ) and bcl w as well as death effectors bax and bak play regulating apoptosis in a tissue specific manner . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
First , Bax was up regulated in maspin transfected prostate and breast tumor cells , whereas the levels of other Bcl 2 family members including Bcl 2 , Bcl xl , and Bak remained unchanged . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The Jurkat R subline that has been shown to be Bax and Bak deficient and resistant to various apoptotic signals was highly sensitive to WGA induced apoptosis . ^^^ However , its mitochondrial component is unrestrained by the loss of Bax and Bak or the upregulation of Bcl 2 expression . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Minocycline induced Bcl 2 , which accumulated in mitochondria and interacted with death promoting molecules including Bax , Bak , and Bid . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The BH 3 only proteins act as sensors for distinct apoptosis pathways , whereas multidomain pro apoptotic Bax and Bak are executioners of death orders relayed by the BH 3 only proteins . 4 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
However , in the presence of CHX , LPS induced release of cytochrome c without modifying steady state levels of Bcl 2 , Bcl xL , Bax , and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We demonstrate constitutive expression of BAX in virtually all embryos at all stages of development , and variable expression of BCL 2 , BCL XL , BCL W , MCL 1 BAK , BAD , BOKL , BID , BIK , and BCL XS . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In few cases ( pro apoptotic factors Bak , Bad and Bax ) , data were in conflict with the previously published stage dependent expression of genes already known to be expressed in male germ cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Interferon ( IFN ) alpha induces a caspase dependent apoptosis that is associated with activation of the proapoptotic Bak and Bax , loss of mitochondrial membrane potential , and release of cytochrome c . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , other proteins of the BCL family are overexpressed in MCL like BCLX , whereas the expression of BAX and BAK was not elevated in MCL . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
RESULTS : Xanthurenic acid at 10 or 20 microM in culture media of human aortic smooth muscle cells induces translocation of the proteins Bax , Bak , Bclxs , and Bad into mitochondria . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Diffuse large B cell lymphomas with germinal center B cell like differentiation immunophenotypic profile are associated with high apoptotic index , high expression of the proapoptotic proteins bax , bak and bid and low expression of the antiapoptotic protein bcl xl . ^^^ Therefore , the bcl6 / CD10 / MUM1 / CD138 differentiation immunophenotypic profiles were studied in relation to ( a ) the apoptotic index , ( b ) the apoptosis associated bcl 2 family proteins bcl 2 , bcl xl , bax , bak , bad and bid , ( c ) the proliferation index ( Ki 67 ) and ( d ) the cell cycle proteins cyclin A , cyclin B 1 , cyclin D 3 , cyclin E , p 53 , Rb , p 16 and p 27 in 79 cases of diffuse large B cell lymphomas . ^^^ The expression of bax , bak and bid and the apoptotic index were significantly higher in the germinal center B cell like profile than in the nongerminal center B cell like profile ( P=0 . 045 , 0 . 018 , 0 . 003 and 0 . 034 , respectively ) . ^^^ The expression of bcl 6 and CD 10 showed significant positive correlation with the expression of bax ( r=0 . 659 , P < 0 . 001 and r=0 . 240 , P=0 . 033 , respectively ) , bak ( r=0 . 391 , P < 0 . 001 and r=0 . 233 , P=0 . 039 , respectively ) and bid ( r=0 . 652 , P < 0 . 001 and r=0 . 238 , P=0 . 035 , respectively ) and significant negative correlation with the expression of bcl xl ( r= 0 . 536 , P < 0 . 001 and r= 0 . 250 , P=0 . 029 , respectively ) . ^^^ The above findings indicate that diffuse large B cell lymphomas with germinal center B cell like immunophenotypic profile are associated with increased apoptosis status , high expression of the proapoptotic proteins bax , bak and bid and low expression of the antiapoptotic protein bcl xl . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In view of the central role of the Bcl 2 family protein in regulating apoptosis , it was tempting to speculate that GCs modulated apoptosis through modulation of the expression of proapoptotic ( Bax , Bcl 10 ( S ) , Bak ) and prosurvival ( Bcl 2 , Bcl 10 ( L ) , Bcl w ) Bcl 2 family members . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Release of the solubilized pool of cytochrome c into the cytosol may then occur by permeabilization of the outer mitochondrial membrane mediated by pro apoptotic Bcl 2 family proteins , notably Bax and Bak , or by Ca2+ triggered mitochondrial permeability transition . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We have characterized the expression of multiple apoptotic proteins in a panel of BL cell lines and describe cell lines with loss of cIAP 1 , cIAP 2 , Bax , Bak , Bcl Xs and p 38 MAP kinase . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This apoptotic process was mediated by the caspase dependent mitochondrial apoptotic pathway as indicated by increased expression and cleavage of caspases 3 and 9 as well as increased expressions of pro apoptotic molecules Bax and Bak . ^^^ Blocking p 53 inhibited HCMV stimulated Bax and Bak expression as well as caspase 3 activation and blocking the ATM pathway inhibited HCMV stimulated p 53 activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
However , the opposite is true for Bax and Bak that promote apoptosis , in part , by increasing the ER Ca ( 2+ ) load and Ca ( 2+ ) transfer from the ER to mitochondria . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
NO * treatment did not alter levels of death receptors 4 and 5 , Fas associated death domain or proapoptotic Bax and Bak proteins in either cell line . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Molecular dynamics study of peptide segments of the BH 3 domain of the proapoptotic proteins Bak , Bax , Bid and Hrk bound to the Bcl xL and Bcl 2 proteins . ^^^ In the current work , these proteins complexed with 10 ( 16BH3 ) , where 10 designates the proapoptotic proteins Bak , Bax , Bid and Hrk , have been modeled in order to establish a pharmacophoric hypothesis that must be present in any ligand capable of binding with the antiapoptotic proteins Bcl 2 and Bcl xL . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cytomegalovirus cell death suppressor vMIA blocks Bax but not Bak mediated apoptosis by binding and sequestering Bax at mitochondria . ^^^ We report that the cytomegalovirus encoded cell death suppressor vMIA binds Bax and prevents Bax mediated mitochondrial membrane permeabilization by sequestering Bax at mitochondria in the form of a vMIA Bax complex . vMIA mutants with a defective mitochondria targeting domain retain their Bax binding function but not their ability to suppress mitochondrial membrane permeabilization or cell death . vMIA does not seem to either specifically associate with Bak or suppress Bak mediated mitochondrial membrane permeabilization . ^^^ Recent evidence suggests that the contribution of Bax and Bak in the mitochondrial apoptotic signaling pathway depends on the distinct phenotypes of cells , and it appears from our data that vMIA is capable of suppressing apoptosis in cells in which this pathway is dominated by Bax , but not in cells where Bak also plays a role . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
For example , a number of genes ( BAD , BAK , BIK , and BAX ) involved in apoptosis were found to be suppressed by methylation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This event occurs independently of several Bcl 2 family proteins , including Bax , Bak and Bcl 2 , and inactivation experiments reveal that the proteolytic activity of caspase 2 is not required for the effect . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
They may include differential expression of death receptors , constitutively active Akt and NFkappaB , overexpression of cFLIP and IAPs , mutations in Bax and Bak genes , and defects in the release of mitochondrial proteins in resistant cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
No correlation was found between the sensitivity of cells to TRAIL and the expression of TRAIL receptors DR 4 and DR 5 , and pro apoptotic proteins Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Treatment of HeLa cells with TPT CuCl ( 2 ) rescues the accumulation of p 53 from the suppression of human papilloma virus E 6 , resulting in a dramatic up regulation of Bax and Bak and down regulation of the antiapoptotic factor Survivin . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
M11L binds constitutively to human Bak and , under some inducible conditions , to human Bax as well , but not to the other Bcl 2 family members ( Bad , Bid , Bcl 2 ) . ^^^ We also demonstrate in coexpression studies that M11L can interact with Bak independently of any involvement with Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Further , silibinin treatment prior to or immediately after UVB exposure altered Bcl 2 , Bax , Bak , and cytochrome c levels in mitochondria and cytosol in favor of or against apoptosis , respectively . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We compared oligodendrocytes of cerebral , cerebellar , and pontine white matter from 5 VWM patients with those of age matched controls by light microscopy and immunohistochemistry using antibodies to activated caspase 3 , bak , bax , bcl 2 , survivin , and Ki 67 , as well as by the TUNEL technique . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Deficiency of Bax and Bak protects photoreceptors from light damage in vivo . ^^^ Photoreceptors of bax ( / ) bak ( / ) but neither bax ( / ) mice nor bak ( / ) mice are protected from developmental apoptosis , suggesting that bax ( / ) bak ( / ) photoreceptors may also be protected from pathologic apoptosis . ^^^ To test this possibility , we exposed bax ( / ) bak ( / ) and bax ( / ) mice to bright light , which normally induces photoreceptor death . ^^^ Photoreceptors in bax ( / ) bak ( / ) mice were protected from death compared to bax ( / ) mice as indicated by a reduction in the number of TUNEL positive photoreceptor nuclei 24 h following light damage and almost complete preservation of photoreceptors 7 days following light damage . ^^^ These results provide the first in vivo evidence that combined deficiency of Bax and Bak can rescue cells from a pathologic stimulus more effectively than Bax deficiency and suggest that combined deficiency of Bax and Bak may also protect cells from other insults . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
RESULTS : Irradiation significantly augmented TRAIL induced apoptosis in prostate cancer cells through upregulation of DR 5 , Bax , and Bak , and induction of caspase activation . ^^^ The sequential treatment of xenografted mice with irradiation followed by TRAIL induced apoptosis through activation of caspase 3 , induction of Bax and Bak , and inhibition of Bcl 2 , and completely eradicated the established tumors with enhanced survival of nude mice . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Antisense transfected cells expressed high levels of Bax and Bak , but low levels of Bcl 2 and Bcl XL when treated with CDDP , peplomycin , 5 fluorouracil or gamma rays . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
METHODS : The parameters reflecting cell proliferation and cell death were studied together with oxidative response , mitochondrial membrane potential ( MMP ) and changes of selected regulatory molecules associated with cell cycle ( p 27 ( Kip 1 ) and p 21 ( Cip1 / WAF1 ) ) and apoptosis ( caspase 3 , caspase 9 , poly ( ADP ribose ) polymerase PARP , Bcl 2 , Bax , Bak , Mcl 1 ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Here we demonstrate that antiapoptotic BCL 2 family proteins promoted tumor formation of transformed baby mouse kidney ( BMK ) epithelial cells by antagonizing BAX and BAK dependent apoptosis . ^^^ An in vitro ischemia system mimicked the tumor microenvironment , and gain of BCL 2 or loss of BAX and BAK was sufficient to confer resistance to apoptosis and to allow for accumulation of polyploid cells in vitro . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast to reported observations in acute promyelocytic leukemia , myeloma cell apoptosis was not associated with either the downregulation of Bcl 2 protein or with alterations in the expression of other Bcl 2 family members , Bax , Bak , Bag , and Bcl xl . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Chlamydia trachomatis infection inhibits both Bax and Bak activation induced by staurosporine . ^^^ We now report that activation of both Bax and Bak , two proapoptotic members of the Bcl 2 family that regulate mitochondrial cytochrome c release , was inhibited in chlamydia infected cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Consistent with these findings , apoptosis induced by phenylurea based compounds was not altered by genetic alterations in the expression of Bcl 2 family proteins that control mitochondria dependent cell death pathways , including over expression of anti apoptotic proteins Bcl 2 or Bcl 10 ( L ) and genetic ablation of pro apoptotic proteins Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Changes in expression of p 53 , Bcl 2 , Bax , and Bak were quantified by Western immunoblotting . ^^^ Apoptosis in both phenotypes occurred with increased expression of p 53 and Bak , but no change in Bcl 2 or Bax . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunohistochemical analysis of bcl 2 , Bax and Bak expression in thyroid glands from patients with Graves ' disease . ^^^ In order to clarify the role of apoptosis and the expression of Bcl 2 family proteins in the pathology of Graves ' disease ( GD ) , we evaluated the apoptosis by in situ end labeling of fragmented DNA and the expression of Bcl 2 , Bax and Bak by immunohistochemistry in thyroid tissues from 20 patients with GD and in normal thyroid tissues from 6 patients with follicular adenoma ( N ) . ^^^ In lymphoid follicles Bcl 2 was expressed in the mantle zone , while Bax and Bak were both expressed in the germinal center . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Despite their resistance to apoptosis , MCMV infected DCs showed Bax to be tightly associated with mitochondria and , together with Bak , forming high molecular weight oligomers , changes normally associated with apoptotic cell death . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Differential involvement of Bax and Bak in TRAIL mediated apoptosis of leukemic T cells . ^^^ We have used TRAIL resistant leukemic cells that are deficient in both Bax and Bak to determine the roles of these Bcl 2 members in TRAIL mediated apoptosis . ^^^ Also , in the absence of Bax and Bak , no release of mitochondrial apoptogenic proteins was observed following TRAIL treatment . ^^^ Adenoviral transduction of the Bax , but not the Bak gene , to the Bax / Bak deficient leukemic cells rendered them TRAIL sensitive as assessed by enhanced apoptotic death and caspase 3 processing . ^^^ These findings demonstrate preferential utilization of Bax over Bak in leukemic cell response to specific apoptotic stimulation . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Treatment with BMS 214662 induced loss of mitochondrial membrane potential ( DeltaPsi ( m ) ) , phosphatidylserine exposure , proapoptotic conformational changes of Bax and Bak , reduction in Mcl 1 levels and activation of caspases 9 and 3 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Chemotherapeutic drugs ( paclitaxel , vincristine , vinblastine , etoposide , doxorubicin , and camptothecin ) significantly augmented TRAIL induced apoptosis in cancer cells through up regulation of DR 4 , DR 5 , Bax , and Bak , and induction of caspase activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Multidomain Bcl 2 homolog Bax but not Bak mediates synergistic induction of apoptosis by TRAIL and 5 FU through the mitochondrial apoptosis pathway . ^^^ Notably , both DU 145 and HCT 116 Bax deficient cells still express Bak . ^^^ Moreover , we show by the use of EGFP tagged Bax and Bak that TRAIL and 5 FU synergistically trigger oligomerization and clustering of Bax but not Bak . ^^^ These data clearly establish distinct roles for Bax and Bak in linking the TRAIL death receptor pathway to the mitochondrial apoptosis signaling cascade and delineate a higher degree of specificity in signaling for cell death by multidomain Bcl 2 homologs . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Here we discuss recent studies demonstrating that the death of antigen activated T lymphocytes during termination of an immune response is initiated by the BH 3 only Bcl 2 family member Bim and also requires its multi BH domain pro apoptotic relatives Bax and Bak . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
A possible mechanism responsible for the different sensitivity in these two cell lines was explored by the examination of Bcl 2 , Bax , Bak , and Fas . ^^^ The cell death stimulus increased anti apoptotic Bcl 2 and decreased pro apoptotic Bcl 2 members ( Bak and Bax ) and Fas in glioblastoma cells deficient in DNA PK . ^^^ Activation of DNA PK is known to promote cell death of human tumor cells via modulation of p 53 , which can down regulate the anti apoptotic Bcl 2 member proteins , induce pro apoptotic Bcl 2 family members and promote a Bax Bak interaction . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expressions of Bax , Bak , and Bcl 2 mRNA in the pancreas were detected by reverse transcriptase polymerase chain reaction ( RT PCR ) on day 3 and at weeks 1 , 2 , 3 , and 4 . ^^^ Meanwhile , Bax and Bak mRNA expression was increased , but Bcl 2 mRNA expression was decreased , as compared with the normal group . ^^^ The administration of losartan resulted in inhibition of acinar cell apoptosis and down regulation of Bax , Bak , and Bcl 2 mRNA expression . ^^^ This action may be associated with its regulation of apoptosis associated genes , such as Bax , Bak , and Bcl 2 mRNA . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The inhibition of apoptosis was associated with a decrease in expression of the proapoptotic molecules , BAK and BAX , and activation of the antiapoptotic phosphatidylinositol 3 kinase ( PI3K ) and AKT pathway , providing potential mechanisms for the effects of RAB 25 on tumor aggressiveness . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression of Bcl 2 , Bcl xl , Bak and Bax proteins in axons of the optic nerve in closed angle glaucoma ] . ^^^ PURPOSE : The aim of our study was the evaluation of Bcl 2 , Bcl xl , Bak and Bax immunoexpression in axons of the optic nerve with absolute glaucoma . ^^^ The samples were immuno stained with antibodies for Bcl 2 , Bak , Bax and Bcl xl protein . ^^^ RESULTS : In our study proapoptotic Bak and Bax protein expression was stronger than antiapoptotic Bcl 2 , Bcl xl protein expression ; Bak / Bcl 2 ( p = 0 . 008 ) , Bax / Bcl 2 ( p = 0 . 0007 ) , Bak / Bcl xl ( p = 0 . 0356 ) , Bax / Bcl xl ( p = 0 . 0077 ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
MATERIALS AND METHODS : The combined immunohistochemical expression levels of the proteins bax , bak , bad , bid , bcl 2 and bcl xl were evaluated by cluster and discriminant analysis . ^^^ RESULTS : Cluster analysis produced : a ) a low expression ( 69 / 79 cases ) and a high expression pro apoptotic cluster ( 10 / 79 cases ) for the combined expression levels of the pro apoptotic proteins bax , bak , bad and bid and b ) a low expression ( 37 / 76 cases ) and a high expression antiapoptotic cluster ( 39 / 76 cases ) for the combined expression levels of anti apoptotic proteins bcl 2 and bcl xl . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
By using rats exposed in utero to the anti androgenic compound flutamide ( 0 . 4 , 2 or 10 mg / kg per day ) , it has been shown that hypospermatogenesis in adult testes could be related to ( 1 ) a long term apoptosis in germ cells but not in somatic Leydig and Sertoli cells as evidenced by the TUNEL approach and ( 2 ) alterations in the mRNA and protein expression of pro ( Bax , Bak , Bid ) and anti apoptotic ( Bcl 2 , Bcl w ) members of the Bcl 2 family . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Whereas Bax or Bak were shown to be required for the proapoptotic effect of Bid , Bcl 2 was described to interfere with its action . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Overexpression of Bcl 2 or Bcl 10 ( L ) , loss of Bax or Bak function , high expression of inhibitor of apoptosis proteins , and reduced release of second mitochondria derived activator of caspases ( Smac / Diablo ) from the mitochondria to the cytosol have all been reported to result in TRAIL resistance in mitochondria dependent type 2 cancer cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The activity of caspase 3 and expression of the proapoptotic proteins Bax , Bad , and Bak were also decreased in neonatal relative to adult neutrophils . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The Bcl 2 family of proteins are well characterized regulators of apoptosis , and the multidomain pro apoptotic members of this family , such as Bax and Bak , act as a mitochondrial gateway where a variety of apoptotic signals converge . ^^^ Although embryonic fibroblasts from Bax / Bak double knockout mice are resistant to apoptosis , we found that these cells still underwent a non apoptotic death after death stimulation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Hexokinase mitochondria interaction mediated by Akt is required to inhibit apoptosis in the presence or absence of Bax and Bak . ^^^ Targeted disruption of mitochondria hexokinase ( HK ) interaction or exposure to proapoptotic stimuli that promote rapid dissociation of hexokinase from mitochondria potently induce cytochrome c release and apoptosis , even in the absence of Bax and Bak . ^^^ These effects are inhibited by activated Akt , but not by Bcl 2 , implying that changes in outer mitochondrial membrane ( OMM ) permeability leading to apoptosis can occur in the absence of Bax and Bak and that Akt inhibits these changes through maintenance of hexokinase association with mitochondria . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bak and Bax are functionally redundant in non neuronal cells and represent a mitochondrial convergence point for cell death signaling pathways . ^^^ Overexpression of N Bak promotes Bax translocation in HeLa cells and induces neuronal cell death in cortical , hippocampal , and cerebellar granule neurons in a Bax dependent manner . ^^^ N Bak interacts with Bcl XL but not BAX , suggesting an indirect mechanism for promoting Bax translocation to the mitochondria . ^^^ The absence of full length Bak expression explains the near exclusive requirement for Bax in neuronal apoptosis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Attenuation of ischemia and / or reperfusion injury during myocardial infarction using mild hypothermia in rats : an immunohistochemical study of Bcl 2 , Bax , Bak and TUNEL . ^^^ Immunohistochemical analysis was carried out using antibodies against Bcl 2 , Bax and Bak . ^^^ In the HT group Bcl 2 was induced in many myocytes , whereas Bax and Bak were induced in only a few myocytes . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cardiolipin is important for the proapoptotic activity of Bcl 2 family members such as Bid , Bax and Bak , and modulation of its metabolism and translocation in mitochondrial membranes could potentially have a strong influence on apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulum . ^^^ Proapoptotic BCL 2 family members BAX and BAK are required for the initiation of mitochondrial dysfunction during apoptosis and for maintaining the endoplasmic reticulum ( ER ) Ca ( 2+ ) stores necessary for Ca ( 2+ ) dependent cell death . ^^^ We found that Bax ( / ) Bak ( / ) double knockout ( DKO ) cells have reduced resting ER Ca ( 2+ ) levels because of increased Ca ( 2+ ) leak and an increase in the Ca ( 2+ ) permeable , hyperphosphorylated state of the inositol trisphosphate receptor type 1 ( IP3R 1 ) . ^^^ BCL 2 and IP3R 1 physically interact at the ER , and their binding is increased in the absence of BAX and BAK . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Differences in mcl 1 , bax , bcl w , bad or bak mRNA levels in infected versus uninfected neutrophils were not remarkable . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In 22 / 36 patients with the pre treatment overexpression of Bax , Bak and Bid proteins , ALT induced a distinct ( more than 50 % from the baseline ) increase in the incidence of apoptosis after 24 h of in vitro treatment . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Whereas proteins such as Bax and Bak play a central role in most forms of apoptosis , the BH 3 only proteins appear to modulate apoptosis through cell type and signal specific pathways . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cotreatment with 17 AAG and SAHA also induced down regulation of Mcl 1 , Bcl xL , and B Raf ; up regulation of Bak ; cleavage of 14 3 3 proteins ; and a profound conformational change in Bax accompanied by translocation to the membrane fraction . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The major antiapoptotic family members , Bcl 10 ( L ) and Bcl 2 , and the major proapoptotic proteins , Bax and Bak , show distinct temporal and spatial patterns of expression in the developing brain . ^^^ Targeted deletions of Bcl 10 ( L ) and Bcl 2 as well as Bax and Bak have proven to be important tools in delineating the process of cell death in the nervous system . ^^^ In contrast , Bax and Bak play redundant roles in regulating the size of the neural progenitor cell population in postnatal mice and in the normal development of the retinal layers of the eye . ^^^ In contrast , excitotoxic cell death is not dependent on either Bax or Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Tumor necrosis factor related apoptosis inducing ligand ( TRAIL ) induces programmed cell death through the caspase activation cascade and translocation of cleaved Bid ( tBid ) by the apical caspase 8 to mitochondria to induce oligomerization of multidomain Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This apoptosis is associated with up regulation and nuclear localization of the tumor suppressor p 53 and activation of mitochondrial apoptosis , which includes up regulation of Bax , Bak , and Pidd , translocation of Bax and caspase 2 onto mitochondria , release of cytochrome c and apoptosis inducing factor , and activation of caspase 9 and caspase 3 . ^^^ This viability preservation results from reduced expression of proapoptotic factors Bax , Bak , and Pidd and from prevention of activation of caspase 2 , 9 , and 3 . ^^^ We conclude that p 53 is a downstream effector of Bruce , and , in response to loss of Bruce function , p 53 activates Pidd / caspase 2 and Bax / Bak , leading to mitochondrial apoptosis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Inhibition of p 38 MAPK by pharmacological inhibitors , dominant negative p 38 , or small interfering RNA , suppressed p53S46P ( but not p53S15P ) , the expression of p 53 inducible genes , the conformational activation of proapoptotic Bax and Bak , the release of cytochrome c from mitochondria , and consequent apoptosis . p38T180 / Y182P was also detected in HIV 1 induced syncytia , in vivo , in patients ' lymph nodes and brains . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
As expected ( ) gossypol induced complete cytochrome c release from mitochondria , increased caspases 3 and 9 activity , and caused apoptotic death without affecting protein levels of Bcl 2 , Bcl 10 ( L ) , Bax , and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of the insulin like growth factor 1 receptor and proapoptotic Bax and Bak proteins in human colorectal cancer . ^^^ To study the relationships between the IGF IR and Bax as well as Bak , 144 cases of colorectal cancer were examined by immunohistochemistry , using the avidin biotin peroxidase method . ^^^ The results were correlated with selected clinicopathological features of colorectal cancer and with the expression of IGF IR , Bax , and Bak in normal colon mucosa . ^^^ In Bax , Bak , or IGF IR positive cancers , the adjacent colorectal mucosa revealed positive immunostaining for these proteins . ^^^ In the majority of Bax , Bak , or IGF IR negative tumors , we observed no staining for these proteins in adjacent mucosa . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The object of our study was to evaluate the expression of the Bcl 2 protein family ( Bcl 2 , Bak , Bax ) , p 53 , proliferating cell nuclear antigen ( PCNA ) , and Ki 67 protein immunoexpression as well as the correlation between the examined markers and some clinicopathological features in papillomas and cancers of conjunctiva and eyelid . ^^^ In the SCP group , p 53 protein expression was observed in 30 cases ( 66 . 6 % ) , Ki 67 in 14 ( 31 . 1 % ) , PCNA in 44 ( 97 . 8 % ) , Bcl 2 in 24 ( 53 . 3 % ) , Bak in 28 ( 62 . 2 % ) , Bax in 31 ( 68 . 9 % ) , and Bcl xl in 11 ( 100 % ) . ^^^ In the SCC group , p 53 protein expression was evaluated in 8 cases ( 72 . 8 % ) , Ki 67 in 2 ( 18 . 2 % ) , PCNA in 8 ( 72 . 7 % ) , Bcl 2 in 5 ( 45 . 4 % ) , Bax and Bak both in 10 ( 90 . 9 % ) , and Bcl xl in 100 % . ^^^ In the BCC group , p 53 protein expression was estimated in 23 cases ( 85 . 1 % ) , Ki 67 in 13 ( 48 . 1 % ) , PCNA in 26 ( 96 . 2 % ) , Bcl 2 in 13 ( 48 . 1 % ) , Bak in 21 ( 77 . 8 % ) , Bax in 22 ( 81 . 5 % ) , and Bcl xl in 23 ( 85 . 2 % ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Humanin binds and nullifies Bid activity by blocking its activation of Bax and Bak . ^^^ HN peptide inhibits tBid induced oligomerization of Bax and Bak in mitochondrial membranes , as shown by experiments with chemical cross linkers or gel filtration . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
There was no considerable difference in the percentage of apoptotic cells in Bak RNAi transfected Bax+ / or Bax / cells treated with curcumin when compared with their corresponding vector transfected cells treated with curcumin . ^^^ The present study demonstrates the role of Bax but not Bak as a critical regulator of curcumin induced apoptosis and implies the potential of targeting antiapoptotic proteins like Bcl XL or overexpression of proapoptotic proteins like Smac as interventional approaches to deal with Bax deficient chemo resistant cancers for curcumin based therapy . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Our evaluation of expression levels of Bcl 2 family members showed increased expression of pro apoptotic Bak and Bax in diabetic rats . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In this study , we show that the coadministration of DNA vaccines encoding human papillomavirus type 16 E 7 with siRNA targeting key proapoptotic proteins Bak and Bax prolongs the lives of antigen expressing dendritic cells in the draining lymph nodes , enhances antigen specific CD 8 ( + ) T cell responses , and elicits potent antitumor effects against an E 7 expressing tumor model in vaccinated mice . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Although the precise mechanism that leads to the permeabilization of mitochondria is still unclear , the activation of multidomain pro apoptotic proteins of the Bcl 2 family , such as Bax and Bak , is evidently crucial . ^^^ Regulation of Bax and Bak by other members of the family has been known for a long time , but recent evidence suggests that additional unrelated proteins participate in the process , both as inhibitors and activators . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Phospho c Jun NH 2 terminal kinase , Bax , Bak , p 21 ( WAF1 / CIP1 ) , caspase 8 , and caspase 3 were examined by immunoblotting . ^^^ Infliximab induced accumulation of reactive oxygen species and up regulation of Bax , Bak , and p 21 ( WAF1 / CIP1 ) proteins , suggesting the involvement of p 53 activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Specifically , we observe that Abeta significantly reduces expression of antiapoptotic Bcl w and Bcl 10 ( L ) , mildly affects expression of bim , Bcl 2 , and bax , but does not alter expression of bak , bad , bik , bid , or BNIP3 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Loss of expression of proapoptotic proteins was observed as follows : Bak , 24 of 41 samples ( 59 % ) ; Bad , 21 of 41 samples ( 51 % ) ; Bid , 20 of 41 samples ( 49 % ) ; Bax , 14 of 41 samples ( 34 % ) ; and Bim / Bod , 2 of 41 samples ( 5 % ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Induction apoptosis of luteolin in human hepatoma HepG 2 cells involving mitochondria translocation of Bax / Bak and activation of JNK . ^^^ We found that Bax and Bak translocated to mitochondria apparently , whereas Fas ligand ( FasL ) was unchanged after a treatment with luteolin for 3 h . ^^^ These data suggest that luteolin induced apoptosis via mechanisms involving mitochondria translocation of Bax / Bak and activation of JNK . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In this model , the simple inhibition of antiapoptotic functions is insufficient to induce apoptosis unless a direct activator of Bax or Bak is present . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 family members Bak and Bax constitute a mitochondrial gateway for multiple death pathways . ^^^ Experiments with Bak and Bax deficient mouse embryonic fibroblasts show that endogenous Bak mediates the effect , whereas Bax is mainly irrelevant . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We have previously correlated Chlamydia trachomatis antiapoptotic activity with the blockade of mitochondrial cytochrome c release and the inhibition of Bax and Bak activation . ^^^ We now report that C . trachomatis infection leads to degradation of Bik , Puma , and Bim , three upstream proapoptotic BH 3 only proteins of the Bcl 2 family that can transmit death signals to mitochondria by inhibiting the Bcl 2 antiapoptotic proteins and / or activating the Bcl 2 proapoptotic members , such as Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Farnesyltransferase inhibitor BMS 214662 induces apoptosis in myeloma cells through PUMA up regulation , Bax and Bak activation , and Mcl 1 elimination . ^^^ BMS 214662 treatment increased levels of the BH 3 only protein PUMA ; induced proapoptotic conformational changes of Bax and Bak ; reduced Mcl 1 levels ; caused mitochondrial transmembrane potential loss ; induced cytochrome c release , caspase activation , apoptosis inducing factor ( AIF ) nuclear translocation , and phosphatidylserine exposure ; and allowed the development of apoptotic morphology . ^^^ However , Z VAD fmk did not prevent BMS 214662 induced Bax and Bak activation and decrease of Mcl 1 levels . ^^^ These results suggest that apoptosis triggered by BMS 214662 is initiated by a PUMA / Bax / Bak / Mcl 1 dependent mechanism . ^^^ In some cell lines , Bax / Bak activation is not sufficient per se to induce mitochondrial failure and release of apoptogenic proteins , and so caspases need to be activated to facilitate apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax and Bak are required for apoptosis induction by sulforaphane , a cruciferous vegetable derived cancer chemopreventive agent . ^^^ Here , we show that multidomain proapoptotic Bcl 2 family members Bax and Bak play a critical role in apoptosis induction by sulforaphane . ^^^ This conclusion is based on the following observations : ( a ) sulforaphane treatment caused a dose and time dependent increase in the protein levels of both Bax and Bak and conformational change and mitochondrial translocation of Bax in SV 40 transformed mouse embryonic fibroblasts ( MEF ) derived from wild type mice to trigger cytosolic release of apoptogenic molecules ( cytochrome c and Smac / DIABLO ) , activation of caspase 9 and caspase 3 , and ultimately cell death ; ( b ) MEFs derived from Bax or Bak knockout mice resisted cell death by sulforaphane , and ( c ) MEFs derived from Bax and Bak double knockout mice exhibited even greater protection against sulforaphane induced cytochrome c release , caspase activation , and apoptosis compared with wild type or single knockout cells . ^^^ Interestingly , sulforaphane treatment also caused a dose and time dependent increase in the protein level of Apaf 1 in wild type , Bax / , and Bak / MEFs but not in double knockout , suggesting that Bax and Bak might regulate sulforaphane mediated induction of Apaf 1 protein . ^^^ In conclusion , the results of the present study indicate that Bax and Bak proteins play a critical role in initiation of cell death by sulforaphane . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Western blot analyses revealed that CT induced an elevation of bcl xL but not bcl 2 or proapoptotic factors bax , bak , and bad . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax dependent regulation of Bak by voltage dependent anion channel 2 . ^^^ Many studies have demonstrated a critical role of Bax in mediating apoptosis , but the role of Bak in regulating cancer cell apoptotic sensitivities in the presence or absence of Bax remains incompletely understood . ^^^ Using isogenic cells with defined genetic deficiencies , here we show that in response to intrinsic , extrinsic , and endoplasmic reticulum stress stimuli , HCT 116 cells show clear cut apoptotic sensitivities in the order of Bax+ / Bak+ > Bax+ / Bak > > Bax / Bak+ > > Bax / Bak . ^^^ Small interference RNA mediated knockdown of Bak in Bax deficient cells renders HCT 116 cells completely resistant to apoptosis induction . ^^^ Surprisingly , however , Bak knockdown in Bax expressing cells only slightly affects the apoptotic sensitivities . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Indeed , bortezomib induced increases of Bik and / or Bim in multiple cell lines but not notably of two other BH 3 only proteins ( Puma and Bid ) nor other family members ( Bax , Bak , Bcl 2 , and Bcl xL ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , the mean conductance of patches of mitochondria indicates MAC activity is present in apoptotic cells deficient in Bax but absent in apoptotic cells deficient in both Bax and Bak . ^^^ These findings indicate Bax is a component of MAC in staurosporine treated HeLa cells and suggest Bax and Bak are functionally redundant as components of MAC . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Proapoptotic BAX and BAK control multiple initiator caspases . ^^^ BAX and BAK operate at both the mitochondria and endoplasmic reticulum ( ER ) to regulate the intrinsic apoptotic pathway . ^^^ An unresolved issue is whether any caspases can be activated in response to intrinsic apoptotic signals in the absence of BAX and BAK . ^^^ Following organelle specific intrinsic stress signals , including DNA damage and ER stress , we detected no activation of CARD containing caspases ( initiator CASP ) 1 , 2 , 9 , 11 and 12 in Bax ( / ) Bak ( / ) doubly deficient ( DKO ) cells . ^^^ Moreover , there was no activation of effector CASP 3 and 7 in DKO cells , consistent with the lack of initiator caspase activity and disfavouring a BAX , BAK independent intrinsic apoptotic pathway to activate initiator caspases . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
They were also associated with up regulation of Bak and a marked conformational change in Bax accompanied by membrane translocation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
These data clearly establish distinct roles for Bax and Bak in linking the TRAIL death receptor pathway to the mitochondrial apoptosis signaling cascade upon DNA damage by IR . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
BH 3 only BIK regulates BAX , BAK dependent release of Ca2+ from endoplasmic reticulum stores and mitochondrial apoptosis during stress induced cell death . ^^^ Release of the mobile ER Ca2+ stores in baby mouse kidney cells doubly deficient in BAX and BAK , on the other hand , is resistant to BIK but is sensitive to ectopic BAK . ^^^ Endogenous cellular BIK , therefore , regulates a BAX , BAK dependent ER pathway that contributes to mitochondrial apoptosis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Additionally , expression of the apoptosis regulating proteins Bax , Bak , Bid , Bcl w , Bcl 2 , XIAP and Mcl 1 was evaluated in B CLL lymphocytes . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Caspase dependent apoptosis induction by phenethyl isothiocyanate , a cruciferous vegetable derived cancer chemopreventive agent , is mediated by Bak and Bax . ^^^ The SV 40 immortalized mouse embryonic fibroblasts derived from Bak and Bax double knockout mice were significantly more resistant to PEITC induced DNA fragmentation compared with wild type or Bak / mouse embryonic fibroblasts . ^^^ CONCLUSION : The results of the present study indicate that caspase dependent apoptosis by PEITC is mediated by Bak and Bax proteins . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bid interaction with cardiolipin primarily orchestrates mitochondrial dysfunctions and subsequently activates Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To characterize the mechanisms of apoptosis induction by proteasome inhibitors , we examined levels of Bcl 2 protein family members ( Bik / NBK , Bax , Bak , Bcl 2 , and Bcl XL ) , release of cytochrome c , and activation of caspase 9 and 3 in human colon cancer cell lines DLD 1 , LOVO , SW 620 , and HCT 116 ; human lung cancer cell line H 1299 ; and human ovarian cancer cell line SKOV 3 after they were treated with bortezomib . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Human cytomegalovirus ( HCMV ) encodes at least two proteins that directly interfere with the apoptotic signaling pathways , viral inhibitor of caspase 8 induced apoptosis vICA ( pUL 36 ) , and mitochondria localized inhibitor of apoptosis vMIA ( pUL 37 10 1 ) . vICA associates with pro caspase 8 and appears to block its recruitment to the death inducing signaling complex ( DISC ) , a step preceding caspase 8 activation . vMIA binds and sequesters Bax at mitochondria , and interferes with BH 3 only death factor / Bax complex mediated permeabilization of mitochondria . vMIA does not seem to either interact with Bak , a close structural and functional homologue of Bax , or to suppress Bak mediated permeabilization of mitochondria and Bak mediated apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Indirect effects of Bax and Bak initiate the mitochondrial alterations that lead to cytochrome c release during arsenic trioxide induced apoptosis . ^^^ Here we used Bak / mouse liver mitochondria and virally immortalized Bax / Bak / mouse embryonic fibroblasts ( MEFs ) to investigate whether or not multidomain proapoptotic BCL 2 family proteins were required for arsenic induced mitochondrial damage and cell death . ^^^ At clinically achievable concentrations , arsenic stimulated cytochrome c release and apoptosis via a Bax / Bak dependent mechanism . ^^^ At higher concentrations ( 125 microM 1 mM ) , cells died via a Bax / Bak independent mechanism mediated by oxidative stress that resulted in necrosis . ^^^ Our data demonstrate for the first time that the cytochrome c release which initiates apoptosis in cells exposed to this classic mitochondrial poison occurs indirectly via the activation of Bax / Bak rather than via direct mitochondrial damage . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
During the process of death receptor mediated apoptosis , Bid is cleaved by activated caspase 8 , and then cleaved Bid conveys apoptotic signals to the mitochondria by activating Bax / Bak . ^^^ D 609 did not interfere with activation of caspase 8 and cleavage of Bid , whereas it blocked cytochrome c release from the mitochondria by inhibiting the activation of Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We also show that tBid decreases CPT 1 activity by a mechanism independent of both malonyl CoA , the key inhibitory molecule of CPT 1 , and Bak and / or Bax , but dependent on cardiolipin decrease . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We first show that PrP is very specific for Bax and can not prevent Bak ( Bcl 2 antagonist killer 1 ) , tBid , staurosporine or thapsigargin mediated cell death . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bak but not Bax is essential for Bcl xS induced apoptosis . ^^^ Here we used embryonic fibroblasts derived from mice deficient in the multidomain proapoptotic members of the Bcl 2 family ( Bax and Bak ) and the apoptotic components of the apoptosome ( Apaf 1 and caspase 9 ) to unravel the cascade of events by which Bcl 10 ( S ) promotes apoptosis . ^^^ Our results show that Bak but not Bax is essential for Bcl 10 ( S ) induced apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cytotoxic chemotherapy upregulates pro apoptotic Bax and Bak in the small intestine of rats and humans . ^^^ Bax and Bak protein and mRNA expression also significantly increased at 6 hours following treatment in rats . ^^^ Bax and Bak protein increased at day 1 after treatment in humans . ^^^ CONCLUSION : Increased expression of Bax and Bak but not other Bcl 2 family members is associated with apoptosis in small intestinal crypts and may amplify the sensitivity and susceptibility of crypt cells to chemotherapy induced enteropathy . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Activation of the TNF R 1 receptor results in the cleavage of BID into truncated BID ( tBID ) , which translocates to the mitochondria and induces the activation of BAX or BAK . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Its three subfamilies have distinct roles : The BH 3 only proteins trigger apoptosis by binding via their BH 3 domain to prosurvival relatives , while the proapoptotic Bax and Bak have an essential downstream role involving permeabilization of organellar membranes and induction of caspase activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Vaccination with dendritic cells transfected with BAK and BAX siRNA enhances antigen specific immune responses by prolonging dendritic cell life . ^^^ Small interfering RNA targeting Bak and Bax antiapoptotic proteins can be used to allow transfected DCs to resist killing by T cells in vivo . ^^^ In this study , we show that human papillomavirus E 7 loaded dendritic cells transfected with BAK / BAX siRNA downregulate Bak and Bax protein expression and become resistant to killing by T cells , leading to enhanced E 7 specific CD8+ T cell activation and antitumor effects in vivo . ^^^ More importantly , we found that vaccination with E 7 loaded DCs transfected with BAK / BAX siRNA was capable of generating a strong therapeutic effect in vaccinated mice , compared with DCs transfected with control siRNA . ^^^ Our data indicate that transfection of dendritic cells with BAK / BAX siRNA represents a plausible strategy for enhancing dendritic cell based vaccine potency . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The overexpression of Bcl xL enhances autophagic cell death when apoptotic cell death is inhibited in Bax ( / ) / Bak ( / ) double knockout cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Using immunohistochemistry the groups were compared for expression of apoptotic proteins : bcl 2 , bcl 10 ( L ) , bax , bak and survivin . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
During VX 944 induced apoptosis , expressions of Bax and Bak were enhanced , and both apoptosis inducing factor ( AIF ) and endonuclease G ( Endo G ) were released from the mitochondria to cytosol , suggesting that VX 944 triggers apoptosis in MM cells primarily via a caspase independent , Bax / AIF / Endo G pathway . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Persistent fetal ocular vasculature in mice deficient in bax and bak . ^^^ OBJECTIVE : To investigate whether proapoptotic Bcl 2 members , Bax and Bak , are involved in fetal vasculature regression . ^^^ METHODS : Adult eyes from mice deficient in Bax and / or Bak were examined grossly and histologically for persistence of fetal vasculature . ^^^ Eyes from postnatal day 7 mice were processed for terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labeling ( TUNEL ) analysis to determine if deficiency of Bax and Bak results in defective developmental apoptosis . ^^^ RESULTS : Only bax ( / ) bak ( / ) eyes retained fetal vasculature into adulthood . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Combined loss of proapoptotic genes Bak or Bax with Bim synergizes to cause defects in hematopoiesis and in thymocyte apoptosis . ^^^ Although it is known that BH 3 only proteins and the multi BH domain proteins , Bak and Bax , are essential for programmed cell death , the overlapping role of these two subgroups has not been examined in vivo . ^^^ To investigate this , we generated Bak / Bim and Bax / Bim double deficient mice . ^^^ We found that although Bax / Bim / , but not Bak / Bim / , mice display webbed hind and front paws and malocclusion of the incisors , both groups of mice present with dysregulated hematopoiesis . ^^^ Combined loss of Bak and Bim or Bax and Bim causes defects in myeloid and B lymphoid development that are more severe than those found in the single knock out mice . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The results showed that MEM induced cell apoptosis involved up regulation of Fas and down regulation of Bcl 2 , DR 3 , DR 4 , TNFRI , and TNFRII in HepG 2 cells , while no changes on the levels of Bax , Bid , Bad , and Bak protein were observed . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The expression levels of Mcl 1 and Bcl XL but not those of Bcl 2 , Bax , and Bak were suppressed by TSA or SK 7041 treatment . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This pathway is regulated by bcl 2 family of anti apoptotic ( bcl 2 , bcl xl , mcl 1 ) and pro apoptotic proteins ( bax , bad , bak ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The results showed that Bcl 2 family molecules , such as Bid , Bak , and Bax , are involved in the parthenolide induced apoptosis and that the defective expression of Bcl 10 ( L ) might contribute to the higher parthenolide sensitivity in the SCK cells than in the other adenomatous cholangiocarcinoma cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Although no significant changes in Bcl 2 expression occurred with ET 1 treatment , the pro apoptotic family members Bad , Bax , and Bak all decreased significantly . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The enhanced TRAIL effect after pretreatment with HDAC inhibitors was consistent with the upregulation of the proapoptotic Bcl 2 family members ( Bim , Bak , Bax , Noxa , and PUMA ) , the downregulation of the anti apoptotic members of the Bcl 2 family ( Bcl 2 and Bcl 10 ( L ) ) , and IAPs . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , antiapoptotic Bcl 2 and Bcl 10 ( L ) levels were increased and pro apoptotic Bax and Bak levels were decreased in the HIF 1alpha overexpressing OSCC line . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Antiapoptotic family proteins such as Bcl 2 and Bcl XL function , at least in part , by binding proapoptotic members such as Bax and Bak and thereby prevent release of the apoptotic cascade of events . `` BH 3 only ' ' members of the family disrupt this interaction by binding , via their BH 3 domain , to a hydrophobic pocket on the surface of the antiapoptotic members . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Essential role of BAX , BAK in B cell homeostasis and prevention of autoimmune disease . ^^^ Here we show proapoptotic BCL 2 family members BAX and BAK are essential for regulating the number of B cells at both immature and mature developmental stages . ^^^ BAX and BAK are critical mediators of B cell death induced by multiple stimuli . ^^^ In addition , BAX and BAK deficient B cells display defective cell cycle progression to B cell receptor crosslinking and lipopolysaccharide , but not to CpG DNA . ^^^ Furthermore , inducible deletion of Bax and Bak in adult mice results in the development of severe autoimmune disease . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Insertion by the activated Bax / Bak in response to DNA damage induces mitochondrial membrane permeabilization ( MMP ) via an anion channel , VDAC in mitochondrial outer membrane that plays a crucial role in releasing small molecules such as cytochrome c , Smac / DIABLO , Omi / HtrA2 , AIF , and endonuclease G leading to cell death . ^^^ Similarly , although etoposide induced apoptosis was inhibited in Bax ( / ) / Bak ( / ) mouse embryonic fibroblasts , autophagy was not inhibited , which was regulated by Bcl xL . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Subsequent studies showed that combined treatment with bortezomib or MG 132 resulted in an increase of death receptor ( DR ) 5 and Bik at protein levels but had no effects on protein levels of DR 4 , Bax , Bak , Bcl 2 , Bcl XL or Flice inhibitory protein ( FLIP ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cleaved or truncated BID ( tBID ) is known to oligomerize both BAK and BAX . ^^^ Previously , BAK and BAX lacing the C terminal fragment ( BAXDeltaC ) were shown to induce modest cytochrome c ( Cyt c ) release from rat brain mitochondria when activated by tBID . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Our results show that the ITCs caused phosphorylation of Bcl 2 , induced mitochondrial translocation of Bak , and disrupted the association of Bcl xl with both Bak and Bax in mitochondrial membrane , indicating that ITC induced mitochondrial damage results at least in part from modulation of select Bcl 2 family members . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Furthermore , the analysis of mice doubly deficient in multidomain Bcl 2 family proteins , Bax and Bak , revealed that apoptosis induced by the BH 3 only protein is completely dependent on Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In contrast , proapoptotic proteins , such as BID , BAX , and BAK , induce Cyt c release independently of the mPT without lysing the MOM . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Antisense RIalpha but not CpG immunomer increased Bax and Bak proapoptotic protein levels and decreased Bcl 2 and RIalpha protein levels in tumor cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Protein protein interactions within the Bcl 2 family are mediated by the helical BH 3 domain of proapoptotic family members , such as Bad , Bak , Bax , or Bid . ^^^ When added to the BH 3 domain derived from other proapoptotic proteins such as Bak , Bax , or Bid , these AEMs significantly increased the Bcl 2 binding affinity of these BH 3 peptides by promoting the helical structure . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bortezomib induced phosphatidylserine exposure , mitochondrial depolarization , ROS generation , Bax and Bak conformational changes , and caspase activation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Caspase 2 was not able to induce cytochrome c release from Bax ( / ) Bak ( / ) mitochondria either . ^^^ In cultured cells , gene deletion of Bax / Bak or Bid abrogated apoptosis induced by overexpression of caspase 2 . ^^^ Collectively , these results indicate that proteolytic activation of Bid and the subsequent induction of the mitochondrial apoptotic pathway through Bax / Bak is essential for apoptosis triggered by caspase 2 . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunoblot analysis revealed that PFE treatment of PC 3 cells resulted in ( 1 ) induction of Bax and Bak ( proapoptotic ) ; ( 2 ) down regulation of Bcl 10 ( L ) and Bcl 2 ( antiapoptotic ) ; ( 3 ) induction of WAF1 / p21 and KIP1 / p27 ; ( 4 ) a decrease in cyclins D 1 , D 2 , and E ; and ( 5 ) a decrease in cyclin dependent kinase ( cdk ) 2 , cdk 4 , and cdk 6 expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Nuclear magnetic resonance determination of the gammaHV 68 5 Bcl 2 structure revealed a BH 3 binding groove that binds BH 3 domain peptides from proapoptotic Bcl 2 family members Bax and Bak via a molecular mechanism shared with host Bcl 2 family proteins , involving a conserved arginine in the BH 3 peptide binding groove . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Although mechanistically different , both transcription independent modes of apoptosis induction converge , as they both initiate permeabilization of the outer mitochondrial membrane via activation of the pro apoptotic Bcl 2 family members Bax or Bak . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Loss of Bif 1 suppresses Bax / Bak conformational change and mitochondrial apoptosis . ^^^ Here , we provide evidence that Bif 1 plays a regulatory role in apoptotic activation of not only Bax but also Bak and appears to be involved in suppression of tumorigenesis . ^^^ Inhibition of endogenous Bif 1 expression in HeLa cells by RNA interference abrogated the conformational change of Bax and Bak , cytochrome c release , and caspase 3 activation induced by various intrinsic death signals . ^^^ While Bif 1 did not directly interact with Bak , it heterodimerized with Bax on mitochondria in intact cells , and this interaction was enhanced by apoptosis induction and preceded the Bax conformational change . ^^^ Taken together , these findings support the notion that Bif 1 is an important component of the mitochondrial pathway for apoptosis as a novel Bax / Bak activator , and loss of this proapoptotic molecule may contribute to tumorigenesis . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Hence , multiple pro survival proteins must be inactivated to unleash Bax and Bak , which drive apoptosis . ^^^ Whether certain BH 3 only proteins also directly activate Bax / Bak remains controversial . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Levels of other Bcl 2 family proteins ( Bcl 2 , Bcl 10 ( L ) , Bad , Bak , Bax ) were unaffected by simultaneous ATRA and TGF beta 1 treatment , when compared to ATRA alone . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , the expression of F1L was essential to inhibit tBid induced cytochrome c release in both wild type murine embryonic fibroblasts ( MEFs ) and Bax deficient MEFs , indicating that F1L could inhibit apoptosis in the presence and absence of Bax . tBid induced Bak oligomerization and N terminal exposure of Bak in Bax deficient MEFs were inhibited during virus infection , as assessed by cross linking and limited trypsin proteolysis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The present study was performed to examine the hypothesis that Stx initiates apoptosis by activating the mitochondrial pathway involving mitochondrial associated , pro apoptotic Bcl 2 family proteins Bax and Bak . ^^^ MATERIALS AND METHODS : To determine if Stx 2 mediated apoptosis is dependent on Bax or Bak , a gene silencing approach was employed using sequence specific small interfering ( si ) RNA duplexes . ^^^ Silencing of Bax and Bak protein expression in human renal proximal tubular epithelial ( HK 2 ) cells and its effect on Shiga toxicity was assessed by immunofluorescence microscopy and Western blotting . ^^^ RESULTS : Transfection of HK 2 cells , shown to be exquisitely sensitive to Stx , with siRNA duplexes successfully diminished Bak , but not Bax protein expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Upregulation of caspase 1 , 2 , 3 , 6 , 7 , 8 , 11 and 12 and upregulation for the transcripts of apoptosis inhibitors bcl 2 , bcl w and bcl 10 and apoptosis promoters ' bax , bak and bad was detected in spleens of sPCV and mPCV mice , but not control mice . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
HDAC inhibitors enhance the apoptosis inducing potential of TRAIL in leukemia cells ( HL 60 , Jurkat , K 562 , and U 937 ) through multiple mechanisms ; up regulation of DR 4 , DR 5 , Bak , Bax , Bim , Noxa and PUMA , down regulation of IAPs , Mcl 1 , Bcl 2 , Bcl XL and cFLIP , release of mitochondrial proteins ( cytochrome c , Smac / DIABLO and Omi / Htr2 ) to the cytosol , induction of p21WAF1 / CIP1 and p27KIP1 , activation of caspase 3 and cleavage of poly ( ADP ribose ) polymerase ( PARP ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Interestingly , Mcl 1 was down regulated as well , although levels of Bax , Bad , or Bak were not altered after treatment with this bispecific antisense oligonucleotide . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Caspase dependent apoptosis induction by guggulsterone , a constituent of Ayurvedic medicinal plant Commiphora mukul , in PC 3 human prostate cancer cells is mediated by Bax and Bak . ^^^ Guggulsterone induced apoptosis was associated with induction of multidomain proapoptotic Bcl 2 family members Bax and Bak . ^^^ On the other hand , SV 40 immortalized mouse embryonic fibroblasts derived from Bax Bak double knockout mice were significantly more resistant to guggulsterone induced cell killing compared with wild type cells . ^^^ In conclusion , the present study indicates that caspase dependent apoptosis by guggulsterone is mediated in part by Bax and Bak . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
This BEA induced apoptosis in human NSCLC A 549 cells was also accompanied by the up regulation of Bax , Bak , and p Bad and down regulation of p Bcl 2 , but no effect on the levels of Bcl 10 ( L ) or Bad proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of pro apoptotic ( p 53 , p 21 , bax , bak and fas ) and anti apoptotic ( bcl 2 and bcl 10 ) proteins in serous versus mucinous borderline ovarian tumours . ^^^ MATERIALS AND METHODS : Immunohistochemical expression of pro apoptotic ( p 53 , p 21 , bax , bak , fas ) and anti apoptotic proteins ( bcl 2 , bcl 10 ) was determined in 34 borderline ( 19 mucinous , 15 serous ) , 20 benign ( 10 mucinous , 10 serous ) and 28 malignant ovarian tumours ( 9 mucinous , 19 serous ) . ^^^ No difference in bax , bak , fas or bcl 10 expression was observed among the three tumour types . ^^^ No difference in p 53 , bax , bak , fas or bcl 10 expression was observed between serous and mucinous borderline ovarian tumours . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In addition , chalcone also triggered the mitochondrial apoptotic signaling by increasing the amount of Bax and Bak and reducing the level of Bcl 2 and Bcl 10 ( L ) , and subsequently activated caspase 9 in MCF 7 and MDA MB 231 cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Western blot analysis indicated that the induction of apoptosis by GA and ursolic acid was accompanied with an activation of caspase 8 and a reduction in the anti apoptotic proteins , Bcl 2 and Bcl xL , although the pro apoptotic proteins , Bax and Bak , remained unaffected . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
While the expression of Bax , Bak , and Bcl 2 was comparable to the wild type cells , the selected clones showed specific up regulation of Bcl XL , an anti apoptotic protein . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The multidomain proapoptotic molecules Bax and Bak are directly activated by heat . ^^^ This permeabilization of the mitochondrial outer membrane depends on activation and oligomerization of multidomain Bcl 2 family proteins Bax or Bak . ^^^ Although specific members of the Bcl 2 family can activate these proapoptotic proteins , we found that heat directly activated Bax or Bak to induce cytochrome c release . ^^^ Compared with wild type cells , bax ( / ) bak ( / ) mouse embryonic fibroblasts and mitochondria isolated from these cells were resistant to heat induced cytochrome c release . ^^^ Cytosol from untreated cells inhibited heat activated Bax or Bak ; however , depletion of cytosolic Bcl xL ablated this protection . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Mcl 1 was critical for the survival of RA synovial fibroblasts , because the forced reduction of Mcl 1 using a Mcl 1 antisense expressing adenoviral vector induced apoptotic cell death , which was mediated through Bax , Bak , and Bim . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Cytotrophoblasts also expressed a 2 fold higher level of p 53 , a 2 fold lower level of 60 kDa Mdm 2 protein , a 2 fold higher level of Bak , but no differences in the expression of 90 kDa Mdm 2 , Bcl 2 , Bcl 10 ( L ) , Mcl 1 , Bax , Bad , and Bad phosphorylated at the serine ( 112 ) , serine ( 136 ) , or serine ( 155 ) sites , compared to the syncytiotrophoblasts . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Engagement of death receptors such as tumor necrosis factor R 1 and Fas brings about the cleavage of cytosolic Bid to truncated Bid ( tBid ) , which translocates to mitochondria to activate Bax / Bak , resulting in the release of cytochrome c . ^^^ In addition to its ability to interact directly with Bax and Bak , tBid also binds Mcl 1 and displaces Bak from the Mcl 1 Bak complex . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The pro apoptotic Bcl 2 family proteins , Bak , Bax , and Bim have been shown to be required for disruption of mitochondria and intrinsic cell death of self reactive B cells whereas the anti apoptotic Bcl 2 , Bcl xL , and Mcl 1 can prevent cell death by interfering with the action of Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Activation of Bak and Bax through c abl protein kinase Cdelta p 38 MAPK signaling in response to ionizing radiation in human non small cell lung cancer cells . ^^^ In this study , we showed that c Abl PKCdelta Rac 1 p38 MAPK signaling is required for the conformational changes of Bak and Bax during ionizing radiation induced apoptotic cell death in human non small cell lung cancer cells . ^^^ Ionizing radiation induced conformational changes and subsequent oligomerizations of Bak and Bax , dissipation of mitochondrial membrane potential , and cytochrome c release from mitochondria . ^^^ Small interference ( siRNA ) targeting of Bak and Bax effectively protected cells from radiation induced mitochondrial membrane potential loss and apoptotic cell death . p 38 MAPK was found to be selectively activated in response to radiation treatment . ^^^ Inhibition of p 38 MAPK completely suppressed radiation induced Bak and Bax activations , dissipation of mitochondrial membrane potential , and cell death . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Importantly , this inducible Bax / M11L interaction is independent of Bak , demonstrated by the complete block of Bax mediated apoptosis in myxoma infected cells that lack Bak expression . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Helicobacter pylori vacuolating cytotoxin induces activation of the proapoptotic proteins Bax and Bak , leading to cytochrome c release and cell death , independent of vacuolation . ^^^ By confocal microscopy , Bax and Bak were activated in AZ 521 cells in which cyto chrome c release was induced by VacA . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
As a consequence , F1L prevents Bak activation , oligomerization and interaction with active Bax , all critical steps in the induction of apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
RT PCR analyses demonstrated an increased level of HO 1 , Mn SOD , Cox 2 , iNOS , TNFalpha , TNFR 1 , IL 1beta , IL 6 , Bax , Bak , and Bad gene expression , while Bcl 2 mRNA expression level decreased . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bcl 2 , Bid , and Bad inhibit assembly sub stoichiometrically , whereas peptides from Bak and Bax promote tubulin polymerization at near stoichiometric concentrations . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
At concentrations that suppress extracellular signal regulated kinase ( ERK ) phosphorylation , BAY 43 9006 dephosphorylates Bad on Ser ( 75 ) and Ser ( 99 ) , activates Bak and Bax , and reduces the mitochondrial transmembrane potential . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The apoptosis in SW 872 human liposarcoma cells induced by quercetin was mediated through the activation of caspase 3 , Bax , and Bak and then cleavage of PARP and downregulation of Bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Role of endoplasmic reticulum depletion and multidomain proapoptotic BAX and BAK proteins in shaping cell death after hypericin mediated photodynamic therapy . ^^^ Apoptosis is rapidly initiated after ER Ca2+ depletion and strictly requires the BAX / BAK gateway at the mitochondria . ^^^ Bax / Bak / double knockout ( DKO ) cells are protected from apoptosis but undergo autophagy associated cell death as revealed by electron microscopy and biochemical analysis . ^^^ Thus , following ER photodamage and consequent disruption of Ca2+ homeostasis , BAX and BAK proteins model PDT mediated cell killing , which is executed through apoptosis in their presence or via an autophagic pathway in their absence . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Specific requirement for Bax , not Bak , in Myc induced apoptosis and tumor suppression in vivo . ^^^ Bax and Bak comprise the mitochondrial gateway for apoptosis induced by diverse stimuli . ^^^ Loss of both bax and bak is necessary to block cell death induced by such stimuli , indicating a great degree of functional overlap between Bax and Bak . ^^^ Using a switchable mouse model of Myc induced apoptosis in pancreatic beta cells , we have shown that Myc induces apoptosis in vivo exclusively through Bax but not Bak . ^^^ Furthermore , blockade of Myc induced apoptosis by the inactivation of Bax , but not Bak , eliminates all restraints to the oncogenic potential of Myc , allowing the rapid and synchronous progression of invasive , angiogenic tumors . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression studies in the yeast S . pombe have been utilised to establish the basis for a genetic analysis designed to identify the lethal partners of the pro apoptotic proteins bak and bax . ^^^ Although bax expression in S . pombe gives rise to a slow growth phenotype , not a lethality , bax expressing cells display the same cell cycle phenotypes described for bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Western blot analysis showed that GW 8510 downregulated the expression of 10 linked inhibitor of apoptosis ( XIAP ) but had no detectable effect on the expression of Bax , Bak , or Bcl 2 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Hepatic mRNA levels were measured for several pro apoptotic adaptors / regulators , including FasL , Fas receptor , FADD , TRADD , Bad , Bak , Bax , and Bcl 10 ( S ) , and anti apoptotic regulators , including Bcl w , Bcl 10 ( L ) , Bcl 2 , and Bfl 1 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We detected time and concentration dependent changes in protein expression of anti apoptotic Bcl 10 ( L ) as well as pro apoptotic Bax and Bak proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
These responses on UVB and / or sanguinarine treatments were associated with ( a ) decrease in Bcl 2 and Bcl 10 ( L ) and ( b ) increase in Bax , Bid , and Bak protein levels . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
MMF treated myeloma cells showed an up regulation of Bak , which most likely together with Bax resulted in the release of cytochrome c . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The apoptosis effector molecules Bax and Bak , Apaf 1 , and caspase 9 were shown to be downstream of p 53 in both pathways . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bak ( and Bax ) to the future ' ' of primary melanoma prognosis . ^^^ Loss of expression of proapoptotic Bcl 2 proteins , namely Bax and Bak , in primary melanomas is associated with a worse long term prognosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
In this study , we demonstrated that NAPS induces apoptosis of Jurkat cells by activating Bak , but not Bax , which are both members of a proapoptotic subfamily of the Bcl 2 proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Immunohistochemistry was employed to examine the expression of the antiapoptotic proteins Bcl 2 and Bcl XL and the proapoptotic proteins Bad , Bak , Bax , Bid , Bim , and p 53 in 21 cases of gastric cancer . ^^^ For the proapoptotic members of the Bcl family , loss of protein expression was observed : Bid ( 14 / 21 cases ; 66 % ) , Bad ( 13 / 21 cases ; 61 % ) , Bax ( 12 / 21 cases ; 57 % ) , Bak ( 9 / 21 cases ; 42 % ) , and Bim ( 4 / 21 cases ; 19 % ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Recent work has demonstrated that heat shock directly activates the apoptotic proteins Bax and Bak , suggesting that these polypeptides function as cellular thermometers in the mitochondrial apoptotic pathway . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Caspase 2 triggers Bax Bak dependent and independent cell death in colon cancer cells treated with resveratrol . ^^^ The activated caspase 2 triggers mitochondrial apoptotic events by inducing conformational changes in Bax / Bak with subsequent release of cytochrome c , apoptosis inducing factor , and endonuclease G . ^^^ Studies using mouse embryonic fibroblasts deficient for both Bax and Bak indicate the contribution of both Bax and Bak in mediating cell death induced by resveratrol and the existence of Bax / Bak independent cell death possibly through caspase 8 or caspase 2 mediated mitochondria independent downstream caspase processing . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Expression of p 53 , p 21 ( WAF 1 ) , Bax , Bak , bcl 2 , as well as total and phosphorylated Cdc 2 in the absence and presence of olomoucine , a phosphorylated Cdc 2 kinase inhibitor , was then determined . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Proapoptotic BAX and BAK modulate the unfolded protein response by a direct interaction with IRE1alpha . ^^^ We investigated UPR signaling events in mice in the absence of the proapoptotic BCL 2 family members BAX and BAK [ double knockout ( DKO ) ] . ^^^ BAX and BAK formed a protein complex with the cytosolic domain of IRE1alpha that was essential for IRE1alpha activation . ^^^ Thus , BAX and BAK function at the ER membrane to activate IRE1alpha signaling and to provide a physical link between members of the core apoptotic pathway and the UPR . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
RESULTS : Etoposide treatment ( 1 ) induced apoptosis in one clone , ES , but not in another clone , ER , ( 2 ) had no effect on the expression of the antiapoptotic proteins Bcl 2 and Bcl 10 ( L ) in both cell clones , whereas the proapoptotic proteins Bak and Bax were dramatically upregulated in ES , but not ER cells , and ( 3 ) induced more extensive processing of procaspase 8 , procaspase 9 , and the caspase 3 targeted substrates , topoisomerase 1 and PARP , in ES cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The latter therapy concept builds on a more detailed understanding of how Bcl 2 like molecules maintain mitochondrial integrity and how BH 3 only proteins and Bax / Bak like molecules can undermine it . ^^^ Means to unleash the apoptotic potential of BH 3 only proteins in tumour cells , or bypass the need for BH 3 only proteins by blocking possible interactions of Bcl 2 like prosurvival molecules with Bax and / or Bak allowing their direct activation , constitute interesting options for the design of novel anticancer therapies . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Activated T cell death requires either of the death effector molecules , Bak or Bax . ^^^ When T cells die , Bak and Bax change their conformations , a phenomenon that is thought to be required for Bak or Bax to drive cell death . ^^^ Here we show that Bak changes conformation before activated T cells die , as detected by an antibody specific for a peptide near the NH 2 terminus of Bak , but Bax does not change its shape markedly until after the cells are dead , as detected by an antibody specific for a peptide near the NH 2 terminus of Bax . ^^^ This latter finding is also true in activated T cells that lack Bak and are therefore dependent on Bax to die . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Apoptosis mediated by the proapoptotic BCL 2 family members BCL 2 associated 10 protein ( BAX ) and BCL 2 antagonist / killer ( BAK ) is part of the antiviral response at the cellular level to limit virus replication . ^^^ These same 5 BCL 2 proteins cooperate with loss of retinoblastoma protein and p 53 tumor suppressor function , by inactivating the BAX and BAK apoptotic pathway to promote epithelial solid tumor growth and resistance to chemotherapy . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The proapoptotic proteins Bax and Bak are required for MOMP , while the antiapoptotic Bcl 2 proteins , including Bcl 2 , Bcl xL , Mcl 1 , and others , prevent MOMP . ^^^ Different proapoptotic BH 3 only proteins act to interfere with the function of the antiapoptotic Bcl 2 members and / or activate Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Tumor sections were analyzed by immunohistochemistry for the expression of regulators of the cell cycle ( p 21 ; retinoblastoma protein ( pRb ) ) , of the intrinsic or extrinsic proapoptotic pathways ( p 53 ; murine double minute gene 2 protein ; tumour necrosis factor related apoptosis inducing ligand ( TRAIL ) R1 / DR4 ; TRAIL R2 / DR5 ) and of Bcl 2 related proteins ( Bcl 2 , Mcl 1 , Bax , Bak , Bok ) , which regulate the common mitochondrial apoptotic pathway . ^^^ In SSM , decrease of Bax and Bak was significantly correlated with a poor prognosis : high Bax was associated with 10 year survival rates of 68 % , whereas low Bax resulted in only 26 % survival , and high Bak was associated with 10 year survival rates of 62 % , whereas low Bak resulted in only 10 % survival . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
To test the role of Bad , Bim , and other proapoptotic Bcl 2 family members in IL 3 withdrawal induced apoptosis , we generated IL 3 dependent cell lines from mice lacking the genes for Bad , Bim , Puma , both Bad and Bim , and both Bax and Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Resveratrol treatment for LNCaP cells was also found to result in a significant ( a ) loss of mitochondrial membrane potential , ( b ) inhibition in the protein level of antiapoptotic Bcl 2 , and ( c ) increase in proapoptotic members of the Bcl 2 family , i . e . , Bax , Bak , Bid , and Bad . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
For pro apoptotic proteins , loss of expression was recorded as follows : Bad 25 % ( 14 / 54 ) , Bak 24 % ( 13 / 54 ) , Bax 42 % ( 23 / 54 ) , Bid 37 % ( 20 / 54 ) , Bim 18 % ( 10 / 54 ) . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Investigation into the mechanisms by which WT 1 regulates apoptosis has revealed that several bcl 2 family members are either direct or indirect WT 1 target genes , including bcl 2 itself , the pro apoptotic family members Bak and Bax , and the anti apoptotic family member Bfl 1 / A1 . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Three groups of the Bcl 2 family proteins can be distinguished : the antiapoptotic proteins , like Bcl 2 and Bcl 10 L , the pro apoptotic members e . g . , Bax , Bak and the BH 3 only proteins . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Our results indicate that 4ICD is functionally similar to BH 3 only proteins , proapoptotic members of the BCL 2 family required for initiation of mitochondrial dysfunction through activation of the proapoptotic multi BH domain proteins BAX / BAK . ^^^ Unique among BH 3 only proteins , however , is the essential requirement of BAK but not BAX to transmit the 4ICD apoptotic signal . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
New work suggests pore formation by homo oligomers of VDAC or hetero oligomers composed of VDAC and pro apoptotic proteins such as Bax or Bak . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We investigated the role of antiapoptotic Bcl xL in the progression of prostate cancer as well as the interactions of Bcl xL with proapoptotic Bax and Bak in androgen dependent and independent prostate cancer cells . ^^^ In vivo interactions of Bcl xL with Bax or Bak in untreated and camptothecin treated LNCaP and PC 3 cells were investigated by means of coimmunoprecipitation . ^^^ In the absence of any stimuli , Bcl xL interacts with Bax and Bak in androgen independent PC 3 cells but only with Bak in androgen dependent LNCaP cells . ^^^ Interactions of Bcl xL with Bax and Bak were also evidenced in lysates from high grade prostate cancer tissues . ^^^ We propose that these interactions may provide mechanisms for suppressing the activity of proapoptotic Bax and Bak in prostate cancer cells and that Bcl xL expression contributes to androgen resistance and progression of prostate cancer . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
The proapoptotic proteins Bak ( Bcl 2 antagonistic killer ) and Bax ( Bcl 2 associated 10 protein ) were depleted in livers from TCPOBOP treated CAR+ / + mice . ^^^ In conclusion , these observations support a prominent role for CAR cytoprotection against Fas mediated hepatocyte injury via a mechanism involving upregulation of Mcl 1 and , likely , downregulation of Bax and Bak . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Its three factions of interacting proteins include the BH 3 only proteins ( e . g . , Bim , Puma , Bad , Noxa ) , which transduce diverse cytotoxic signals to the mammalian pro survival proteins ( Bcl 2 , Bcl 10 ( L ) , Bcl w , Mcl 1 , A 1 ) , whereas Bax and Bak , when freed from pro survival constraint , provoke the mitochondrial permeabilization that triggers apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
We show that GT induces apoptotic cell death by activating the proapoptotic Bcl 2 family member Bak , but not Bax , to elicit the generation of reactive oxygen species , the mitochondrial release of apoptogenic factors , and caspase 3 activation . ^^^ Activation of Bak by GT is direct , as GT triggers in vitro a dose dependent release of cytochrome c from purified mitochondria isolated from wild type and Bax but not Bak deficient cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bax interacting factor 1 ( Bif 1 ) interacts with both Bax and Bak that are essential for the intrinsic pathway of apoptosis , and enhances apoptosis . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Gossypol induces Bax / Bak independent activation of apoptosis and cytochrome c release via a conformational change in Bcl 2 . ^^^ Cells without Bak and Bax are largely resistant to apoptosis , despite the presence of other key components of the apoptotic machinery . ^^^ We screened 7 , 800 natural compounds and found several that could specifically induce caspase activation and the release of cytochrome c ( cyto c ) in the bak ( / ) / bax ( / ) cells . ^^^ We found that gossypol , but not other Bcl 2 interacting molecules , induced cyto c release and loss of mitochondrial membrane potential ( delta psi m ) independently of mPTP and Bak / Bax activation . ^^^ Furthermore , we found that gossypol induced an allosteric change in Bcl 2 in both bak ( / ) / bax ( / ) cells and Bcl 2 overexpressing cells . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Role of Bax and Bak in mitochondrial morphogenesis . ^^^ Two members of the Bcl 2 family , Bax and Bak , change intracellular location early in the promotion of apoptosis to concentrate in focal clusters at sites of mitochondrial division . ^^^ Here we report that in healthy cells Bax or Bak is required for normal fusion of mitochondria into elongated tubules . ^^^ Our results show that Bax and Bak regulate mitochondrial dynamics in healthy cells and indicate that Bcl 2 family members may also regulate apoptosis through organelle morphogenesis machineries . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Critical role for mitochondrial oxidative phosphorylation in the activation of tumor suppressors Bax and Bak . ^^^ BACKGROUND : Activation of Bax and Bak , which act to permeabilize the mitochondrial membrane , is an essential step in the cell death response and therefore in the suppression of tumorigenesis . ^^^ METHODS : Bax and Bak activation ( conformational change and dimerization ) was monitored in Rat 1 fibroblasts and human cancer cells subjected to endoplasmic reticulum ( ER ) stress , DNA damage , or tumor necrosis factor alpha ( TNF alpha ) treatment . ^^^ Pharmacologic inhibitors of reactive oxygen species production , electron transport in the respiratory chain , oxidative phosphorylation , and appropriate controls were used to identify potential modes by which Bax and Bak activation and the cell death response are controlled . ^^^ The oligomerization state of Bax and Bak was determined by cross linking and subsequent immunoblot analysis ; Bax conformational change was analyzed by immunoprecipitation and immunoblotting with an antibody specific for the active conformation . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
Bak and Bax are in the Bcl 2 family and counteract the antiapoptotic function of Bcl 2 . ^^^ We hypothesized that ( a ) survival benefit in HRPC patients treated with taxanes is determined by the presence of Bcl 2 protein and ( b ) altered expression of Bak and Bax protein caused by genetic mutation is associated with biological aggressiveness of prostate cancer . ^^^ Surgical specimens of localized prostate cancer and biopsy specimens of HRPC were used for immunostaining of Bcl 2 , Bak , and Bax as well as DNA extraction . ^^^ Mutations in the Bak and Bax genes were screened by single strand conformational polymorphism , and confirmed by direct DNA sequencing . ^^^ Mutation of the Bak and Bax genes is a rare event in prostate cancer . . ^^^
Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
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Interacting proteins: Q07812 and Q16611	Pubmed	SVM Score :0.0
NA