Pubmed abstracts for Protein-Protein Interaction search result :


Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
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Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
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Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
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Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
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Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
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Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
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Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
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Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
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Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
In contrast to Bax , a proapoptotic Bcl 2 gene , ANT 1 was unable to elicit a form of cell death in yeast . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
However , other proteins including Bcl 2 , BAX and virus derived proteins may interact with the ANT to regulate the MPTP . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
The ANT preparations used were free of porin , cyclophilin D , and Bax as analysed immunologically and by activity measurements . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Immunodepletion of Bax from PTPC or purification of PTPC from Bax deficient mice yielded a PTPC that could not permeabilize membranes in response to atractyloside , a proapoptotic ligand of the adenine nucleotide translocator ( ANT ) . ^^^ Bax and ANT coimmunoprecipitated and interacted in the yeast two hybrid system . ^^^ Ectopic expression of Bax induced cell death in wild type but not in ANT deficient yeast . ^^^ Recombinant Bax and purified ANT , but neither of them alone , efficiently formed atractyloside responsive channels in artificial membranes . ^^^ Hence , the proapoptotic molecule Bax and the constitutive mitochondrial protein ANT cooperate within the PTPC to increase mitochondrial membrane permeability and to trigger cell death . . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Vpr favors the permeabilization of artificial membranes containing the purified PTPC or defined PTPC components such as the adenine nucleotide translocator ( ANT ) combined with Bax . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Bax and adenine nucleotide translocator ( ANT ) , the most abundant inner mitochondrial membrane protein , can interact in artificial lipid bilayers to yield an efficient composite channel whose electrophysiological properties differ quantitatively and qualitatively from the channels formed by Bax or ANT alone . ^^^ Cooperative channel formation by Bax and ANT is stimulated by the ANT ligand atractyloside ( Atr ) but inhibited by ATP , indicating that it depends on the conformation of ANT . ^^^ In contrast to the combination of Bax and ANT , ANT does not form active channels when incorporated into membranes with Bcl 2 . ^^^ Bcl 2 prevents channel formation by Atr treated ANT and neutralizes the cooperation between Bax and ANT . ^^^ Our data are compatible with a mnage  trois model of mitochondrial apoptosis regulation in which ANT , the likely pore forming protein within the PTPC , interacts with Bax or Bcl 2 which influence its pore forming potential in opposing manners . . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
However , it has been reported that it is adenine nucleotide translocator ( ANT ) with which Bax / Bcl xL interacts that modulate the channel activity . ^^^ Here , we investigated the role of ANT and VDAC in the changes of isolated mitochondria triggered by Bax and by chemicals that induce permeability transition ( PT ) . ^^^ In rat and yeast mitochondria , Bax did not affect the ADP / ATP exchange activity of ANT . ^^^ VDAC deficient but not ANT deficient yeast mitochondria showed resistance to cytochrome c release , Deltapsi loss , and swelling caused by Bax and PT inducers . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
The PTPC is formed in the IM / OM contact site and contains the two most abundant IM and OM proteins , adenine nucleotide translocator ( ANT , in the IM ) and voltage dependent anion channel ( VDAC , in the OM ) , the matrix protein cyclophilin D , which can interact with ANT , as well as apoptosis regulatory proteins from the Bax / Bcl 2 family . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Full length Bid preferentially permeabilizes membranes and induces the formation of large conductance channels at neutral pH , when added to liposomes or bilayers containing both purified ANT and Bax , yet has no or little effect combined with ANT or Bax alone . t Bid acts on membranes containing ANT alone with the same efficiency as on those containing both ANT and Bax . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Further , in postischemic caudate putamen in vivo and in isolated brain mitochondria in vitro , the authors found enhanced heterodimerization between Bax and the mitochondrial membrane permeabilization related proteins adenine nucleotide translocator ( ANT ) and voltage dependent anion channel . ^^^ The ANT inhibitor bongkrekic acid prevented Bax and ANT interactions and inhibited Bax triggered caspase 9 release from isolated brain mitochondria in vitro . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Peptides corresponding to the BH 3 domains of Bax ( BaxBH 3 ) or Bcl 2 ( Bcl2BH3 ) are potent inducers of apoptosis when fused to the Atennapedia plasma membrane translocation domain ( Ant ) . ^^^ Thus , BaxBH 3 might induce MMP via an action on at least two targets , ANT and Bax like proteins . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
This was shown by loading the vesicles with malate that was not liberated by Bax AC . ( 3 ) The Bax AC effect was dependent on a specific association of cytochrome c with the porin ANT complex , as dissociation of the complex by bongkrekate abolished the Bax dependent cytochrome c liberation . ( 4 ) The Bax AC effect was as well suppressed by hexokinase phosphorylating glucose . . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Conversely , Bax , which displaces Bcl 2 from ANT in apoptotic cells , inhibits ADP / ATP exchange through a direct action on ANT . ^^^ The Bax mediated inhibition of ADP / ATP exchange can be separated from Bax stimulated formation of nonspecific pores by ANT . ^^^ These data are compatible with a model of mitochondrial apoptosis regulation in which ANT interacts with either Bax or Bcl 2 , which both influence ANT function in opposing manners . ^^^ Bcl 2 would maintain the translocase activity at high levels , whereas Bax would inhibit the translocase function of ANT . . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Parallel to these observations , ultrastructural analysis in the 5 HT2B receptor knockout mice heart revealed pronounced mitochondrial defects in addition to altered mitochondrial enzyme activities ( cytochrome oxidase and succinate dehydrogenase ) and ANT 1 and Bax expressions . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
If the VDAC binding site is not occupied by hexokinase , the VDAC ANT complex has two critical qualities : firstly , Bax gets access to cytochrome c and secondly the ANT is set in its c conformation that easily changes conformation into an unspecific channel ( uniporter ) causing permeability transition . ^^^ Activity of bound hexokinase protects against both , it hinders Bax binding and employs the ANT as anti porter . ^^^ This firstly restrains interaction between VDAC and ANT and secondly changes the VDAC structure into low affinity for hexokinase and Bax . ^^^ Cytochrome c in the creatine kinase complex will be differently organised , not accessible to Bax and the ANT is run as anti porter by the active creatine kinase octamer . ^^^ However , when , for example , free radicals cause dissociation of the octamer , VDAC interacts with the ANT with the same results as described above : Bax dependent cytochrome c release and risk of permeability transition pore opening . . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
If the VDAC binding site is not occupied by hexokinase , the VDAC ANT complex has two critical qualities : firstly , external Bax gets access to the cytochrome c and secondly the ANT stays in the c conformation that easily changes the structure to an unspecific uni porter causing permeability transition . ^^^ Activity of bound hexokinase protects against both , it hinders Bax binding and employs the ANT as specific anti porter . ^^^ This firstly hinders direct interaction between VDAC and ANT and secondly changes porin structure into low affinity for hexokinase and external Bax . ^^^ Cytochrome c in the creatine kinase complex will be differently organised not accessible to Bax and the ANT is run as anti porter by the active octamer . ^^^ However , when free radicals cause dissociation of the octamer , VDAC interacts with the ANT with the same results as described above : Bax dependent cytochrome c release and risk of permeability transition pore opening . . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
Data have shown that Ant per se inhibited BAX translocation from cytosol to mitochondria and retained cytochrome C in the mitochondria , whereas LA induced cytochrome C release . ^^^ We conclude that Ant inhibits apoptosis in preovulatory follicles through a decrease of BAX translocation to mitochondria , suggesting that GnRH may act as a physiological intraovarian modulator factor that is able to interfere with follicular development through an increase in apoptotic events mediated by an imbalance among the BCL 2 family members . . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
CONCLUSION : Development of S negative cells and reduced endogenous and radiation induced ROS coupled with higher levels of anti ( Bcl 2 ) as well as pro ( Bax ) apoptotic regulators observed in spheroids suggest the intricate / complex nature of endogenous as well as induced stress resistance that could exist in tumors , which contribute to the treatment resistance . . ^^^
Interacting proteins: Q07812 and P12235 Pubmed SVM Score :0.0
EGF increased the expression of the Bcl 10 ( L ) protein , an antiapoptotic member of the Bcl 2 family , but not that of other anti ( Bcl 2 ) or proapoptotic ( Bad and Bax ) protein members . ^^^