Pubmed abstracts for Protein-Protein Interaction search result :

Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Inhibition of PI3K , mTOR and MEK signaling pathways promotes rapid apoptosis in B lineage ALL in the presence of stromal cell support . ^^^ In this study , we have made use of small molecular weight inhibitors and an established stromal cell dependent pre B ALL cell line , BLIN 2 , to investigate the role of the MAP kinase , PI3K / Akt , JAK / STAT and mTOR pathways in the promotion of leukemic cell growth in the presence of stromal cell support . ^^^ Our data suggest that stromal cell mediated apoptotic protection in B lineage ALL is mediated by PI3K / mTOR and MEK via a synergistic mechanism ( s ) . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
The phosphatidyl inositol 3 kinase ( PI3k ) / Akt pathway has been implicated in childhood acute lymphoblastic leukemia ( ALL ) . ^^^ In conclusion , rapamycin targets 2 pathways that are crucial for cell survival and chemoresistance of malignant lymphoblasts PI3k / Akt through the mammalian target of rapamycin and NF kappaB through FKBP 51 suggesting that the drug could be beneficial in the treatment of childhood ALL . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
The p 85 alpha subunit contains a NH 2 terminal src homology ( SH ) 3 domain , a region with homology to the product of the breakpoint cluster region ( bcr ) gene , and a COOH terminal portion of the molecule which contains two SH 2 domains , separated by a spacer region . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
These cDNAs were demonstrated to encode a 55 kDa protein ( p55alpha ) containing two SH 2 domains and an inter SH 2 domain of p85alpha but neither a bcr domain nor a SH 3 homology domain . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
This 50 kDa protein contains two SH 2 domains and an inter SH 2 domain of p85alpha , but the SH 3 and bcr homology domains of p85alpha were replaced by a unique 6 amino acid sequence . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
In this study , we provide evidence that coligation of FcgammaRIIb 1 with BCR induces binding of PI3K to SHIP . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Upon treatment with CGP 57148 , CRKL , a specific substrate for BCR ABL that propagates signals via phosphatidylinositol 3 ' kinase ( PI3K ) , was dephosphorylated , indicating inhibition of BCR ABL tyrosine kinase at the cellular level . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Membrane translocation of PKB and subsequent PKB activation are dependent on BCR activation of phosphatidylinositol 3 kinase ( PI3K ) . ^^^ However , under conditions of continuous PI3K activation or BCR triggering there is only transient recruitment of PKB to the plasma membrane , indicating that there must be a molecular mechanism to dissociate PKB from sites of PI3K activity in B cells . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
We have recently reported that simultaneous inhibition of the MEK and PI3K pathways or the MEK and mTOR pathways promote rapid apoptosis of the stromal cell dependent B lineage ALL cell line BLIN 2 in the presence of stromal cell support . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Whereas CD 19 does not appear to be involved in this SYK dependent pathway , the SYK substrate CBL is likely involved as the dominant negative SYK markedly attenuates CBL tyrosine phosphorylation and completely blocks the BCR dependent association of CBL with p 85 PI3K . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Thus , Bam 32 represents a novel B cell associated adaptor that regulates BCR signaling downstream of PI3K . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
BCR engagement initiates several signaling events such as activation of PLCgamma , Ras , and PI3K , which generally speaking , lead to survival . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
A prominent feature of CD 19 signaling is the binding and activation of phosphoinositide 3 kinase ( P13K ) , which accounts for the majority of PI3K activity induced by BCR ligation . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Studies of mice deficient in components of the PI3K and PLCgamma pathways demonstrate that these pathways play critical roles in both pre BCR and BCR dependent selection events during B cell differentiation . ^^^ Taken together , the present data clearly indicate that PI3K and PLCgamma play critical and indispensable roles in the signal transduction cascades leading to multiple biological responses downstream of the BCR . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
In this review , we discuss the role of phosphatidylinositol 3 kinase ( PI3K ) and Rap 1 in B cell receptor ( BCR ) signaling . ^^^ In addition to Akt , PI3K derived lipids also regulate the activity and localization of other targets of BCR signaling . ^^^ Thus , a key event in BCR signaling is the recruitment of PI3K to the plasma membrane where its substrates are located . ^^^ The docking proteins that the BCR uses to recruit PI3K include CD 19 , Cbl , Gab 1 , and perhaps Gab 2 . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Hence , these data suggest that BCAP bridges BCR associated kinases to the PI3K pathway by regulating PI3K localization . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
By overexpressing Gab 1 in the WEHI 231 B cell line , we found that Gab 1 can potentiate BCR induced phosphorylation of Akt , a PI3K dependent response . ^^^ Moreover , using confocal microscopy , we show that BCR ligation can induce the translocation of Gab 1 from the cytosol to the plasma membrane and that this requires the Gab 1 PH domain as well as PI3K activity . ^^^ These findings are consistent with a model in which the binding of the Gab 1 PH domain to PI3K derived lipids brings Gab 1 to the plasma membrane , where it can be tyrosine phosphorylated and then act as an amplifier of BCR signaling . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
While the function of PI3K has been largely attributed to the generation of D 3 lipids , an unanswered question has been whether p 85 with a number of motifs ( SH 2 , SH 3 , BcR homology ( BH ) region ) can generate independent intracellular signals . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Bruton ' s tyrosine kinase ( Btk ) acts downstream of phosphoinositide 3 kinase ( PI3K ) in a pathway required for B cell receptor ( BCR ) dependent proliferation . ^^^ Only about 5 % of the BCR dependent gene expression changes were significantly affected by reduced PI3K or Btk . ^^^ These data are consistent with PI3K acting through Btk and other effectors to regulate expression of a critical subset of BCR target genes that determine effective entry into the cell cycle . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
We have previously shown that B cell Ag receptor ( BCR ) signaling leads to activation of PI3K and Akt as well as inhibition of GSK 3 . ^^^ Therefore , we hypothesized that BCR engagement would induce the accumulation of beta catenin via a PI3K / Akt / GSK 3 pathway . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Blockade of phosphatidylinositol 3 kinase ( PI3K ) activity completely abolished BCR induced recruitment of TAPP 1 and TAPP 2 , while expression of active PI3K is sufficient to drive constitutive membrane localization of TAPP 1 and TAPP 2 . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Here we demonstrate that phosphoinositide 3 kinase ( PI3K ) inhibitors preclude antigen presentation induced by BCR or Igbeta but not Igalpha . ^^^ Rather PI3K inhibitors block de novo formation of a multivesicular antigen processing compartment , which is induced by triggering of the BCR or Igbeta . ^^^ Strikingly , we found using fluorescent probes binding specifically to PI3K products that BCR and Igbeta but not Igalpha induce PI3K activation in endocytic compartments wherein antigen is transported . ^^^ Altogether , these results strongly suggest that Igbeta couples the BCR to PI3K activation that is instrumental for de novo formation of the antigen processing compartment and efficient antigen presentation . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
However , through analysis of PI3K / and Btk / mice , B cell antigen receptor ( BCR ) induced activation of Btk in mouse B cells was found to be unaffected by PI3K inhibitors or by a lack of PI3K . ^^^ Transgenic expression of Bcl xL restored the development and BCR induced proliferation of B cells in PI3K / mice . ^^^ Our results indicate that PI3K and Btk have unique roles in proximal BCR signaling and that they have a common target further downstream in the activation of NF kappaB . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
BCR targets cyclin D 2 via Btk and the p85alpha subunit of PI 3 K to induce cell cycle progression in primary mouse B cells . ^^^ The p85alpha subunit of PI 3 K and Btk are two crucial components of the B cell receptor ( BCR ) signalling pathway . ^^^ In the present study , we showed that primary splenic B cells from p85alpha null and xid ( Btk deficient ) mice fail to induce cyclin D 2 expression and enter early G 1 , but not S phase of the cell cycle in response to BCR engagement . ^^^ Furthermore , these Btk or p85alpha null B cells displayed increased cell death compared with wild type following BCR engagement . ^^^ Collectively , these data provide evidence for the concept that the B cell signalosome ( p85alpha , Btk , BLNK and PLCgamma ) is involved in regulating cyclin D 2 expression in response to BCR engagement . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Because Ras can activate the Raf 1 / ERK pathway and the phosphatidylinositol 3 kinase ( PI3K ) / Akt pathway , we asked whether Rap activation limits the ability of the BCR to signal via these pathways . ^^^ Thus activation of endogenous Rap by the BCR limits BCR induced activation of the PI3K / Akt pathway , opposes the subsequent inhibition of the FKHR / p27Kip1 pro apoptotic module , and enhances BCR induced cell death . ^^^ Consistent with the idea that Rap GTP is a negative regulator of the PI3K / Akt pathway , expressing constitutively active Rap 2 ( Rap2V12 ) reduced BCR induced phosphorylation of Akt and FKHR . ^^^ Finally , our finding that Rap2V12 can bind PI3K and inhibit its activity in a manner that depends upon BCR engagement provides a potential mechanism by which Rap GTP limits activation of the PI3K / Akt pathway , a central regulator of B cell growth and survival . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Comparison of Burkitt ' s lymphoma derived Akata , Mutu 1 , and Daudi cells , which are representative responders and nonresponders to BCR mediated EBV activation , respectively , indicated that three signaling pathways , phosphatidylinositol 3 kinase ( PI3K ) , extracellular signal regulated kinase ( ERK ) , and p 38 mitogen activated protein kinase ( MAPK ) , were activated in anti Ig treated Akata and Mutu 1 cells . ^^^ Transfection assays in EBV negative Daudi cells revealed that PI3K activated a promoter for BZLF 1 , which is a switch of EBV activation from a latent infection , in the absence of other EBV products suggesting that the BZLF promoter was a target of BCR signaling , and that PI3K was important for BCR mediated BZLF 1 activation . ^^^ These results indicate that the absence of PI3K impedes the progression of signals through the BCR and becomes a determinant of unresponsiveness to BCR mediated EBV activation . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
In contrast to studies with PI 3K inhibitors , which inhibit all classes of PI 3Ks , the p85alpha regulatory subunit is not required for BCR induced MEK1 / 2 and p42 / 44ERK phosphorylation , suggesting the contribution of another PI 3K family members in MEK1 / 2 and p42 / 44ERK activation . ^^^ However , p85alpha ( / ) splenic B cells are defective in BCR induced IkappaB kinase beta and IkappaBalpha phosphorylation . ^^^ We demonstrate that NF kappaB signaling is required for cyclin D 2 induction via the BCR in normal B cells , implicating a possible link with the defective IkappaB kinase beta and IkappaBalpha phosphorylation in p85alpha ( / ) splenic B cells and their ability to induce cyclin D 2 . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Phosphatidylinositol 3 kinase ( PI3K ) , which has been suggested to associate with and become activated by Bcr Abl , has been shown to be required for Bcr Abl mediated cell growth . ^^^ First , we confirmed that expression of p 185 ( bcr abl ) in HL 60 cells , which renders these cells resistant to apoptosis , induces tyrosine phosphorylation of the p 85 subunit of PI3K . ^^^ Consistent with this result , we observed a 20 fold increase in PI3K activity upon immunoprecipitation of tyrosine phosphorylated proteins from cells expressing Bcr Abl versus control cells . ^^^ Nevertheless , treatment of HL 60 . p185 ( bcr abl ) cells with wortmannin , a potent inhibitor of PI3K , eliminated PI3K activity but did not interfere with the resistance of these cells to apoptosis . ^^^ We conclude that while PI3K participates in the anti apoptotic response mediated by some growth factors and also seems to be important for the growth of Bcr Abl positive cells , it does not play any role in Bcr Abl mediated resistance to apoptosis . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Bam 32 is an adaptor protein recruited to the plasma membrane upon B cell receptor ( BCR ) crosslinking in a phosphoinositol 3 kinase ( PI3K ) dependent manner ; however , its physiologic function is unclear . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Furthermore , treatment of cells with specific PK inhibitors known to be involved in serine phosphorylation of Bad ( LY 294002 for PI3K and H 89 for PKA ) mimiced or enhanced BCR induced cell death . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
BCR engagement was recently shown to induce a drop in phosphatidylinositol 3 kinase ( PI3K ) / Akt signaling , preceding the increase in p 27 . ^^^ We demonstrate that pharmacologic inhibitors of PI3K or BCR engagement lead to decreased inactive cytoplasmic levels and increased active functional nuclear FOXO3a . ^^^ Ectopic c Myc blocked the induction of p 27 expression upon either inhibition of PI3K or BCR engagement . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Stimulation of B cells through the B cell antigen receptor ( BCR ) leads to the activation of numerous intracellular signaling pathways including phosphoinositide ( PI ) 3 kinases ( PI3K ) . ^^^ Gene targeting experiments had shown that B cells deficient in p85alpha , an adaptor protein required for PI3K function , were defective in their ability to proliferate in response to BCR stimulation . ^^^ Unexpectedly , they show that while the BCR induced phosphorylation of the PI3K dependent kinase Akt is reduced in p85alpha deficient cells , the phosphorylation of two downstream targets of Akt FOXO 1 and ribosomal protein S 6 is largely unaffected . ^^^ In this issue of the European Journal of Immunology , Hess et al . report analysis of intracellular signaling pathways in p85alpha deficient B cells and show that in the absence of p85alpha there is a partial impairment in BCR induced calcium flux , and a reduction in activation of the transcription factor NF kappaB . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
B cell receptor ( BCR ) driven proliferation is completely blocked either in cells lacking the p85alpha regulatory isoform of PI3K or in wild type cells treated with pharmacological PI3K inhibitors . ^^^ Notably , addition of phorbol ester restores BCR mediated proliferation in p85alpha deficient cells but not wild type cells treated with PI3K inhibitors . ^^^ These findings suggest that the primary BCR signaling defect in B cells lacking p85alpha is a failure to activate diacylglycerol regulated signaling enzymes , most likely protein kinase C . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
BCR activation of PI3K is Vav independent in murine B cells . ^^^ However , pharmacological inhibition of PI3K by wortmannin or deletion of the p110delta catalytic subunit has no effect on Vav activation in response to BCR engagement , suggesting that this mechanism does not operate in vivo . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
The signaling enzyme phosphoinositide 3 kinase ( PI3K ) is activated following B cell receptor ( BCR ) engagement and by many other receptors on B lymphocytes . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Here , we show that RhoA is activated , downstream of PI3K , in response to BCR stimulation and is important for BCR dependent calcium flux and cell proliferation . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
We found that treatment with IL 4 , but not other cytokines , affected subsequent BCR signaling by creating a new pathway in which the need for PI3K in ERK activation was eliminated . ^^^ As in the classical pathway , BCR induced ERK activation in the new , PI3K independent pathway required MEK and was reflected in c Raf . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
RESULTS : The VH mutation subgroups were characterized by a differential expression of the BCR associated genes ZAP 70 and PI3K . ^^^ The 17p subgroup showed an additional down regulation of BCR associated genes such as SYK and PI3K . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
B cell receptor ( BCR ) cross talk : CD 40 engagement creates an alternate pathway for BCR signaling that activates 1 kappa B kinase / I kappa B alpha / NF kappa B without the need for PI3K and phospholipase C gamma . ^^^ Interruption of several mediators that constitute the signalosome , such as PI3K and phospholipase Cgamma 2 , completely blocks BCR signaling for NF kappaB . ^^^ Through this alternate pathway BCR triggering induces nuclear NF kappaB without the need for PI3K or for phospholipase Cgamma 2 . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
The inhibitors of PI3K activity , LY 294002 and Wortmannin , also abrogate cyclin D 2 induction by BCR cross linking , confirming that the class IA PI3K is necessary for cyclin D 2 induction in response to BCR stimulation . ^^^ Furthermore , using both p85alpha null and p110delta null B cells and inhibitors of PI3K , this study demonstrates for the first time , that BCR cross linking induces cyclin D 2 mRNA expression via transcriptional activation of the cyclin D 2 promoter and that this transcriptional activation of cyclin D 2 requires PI3K activity . ^^^ Further characterisation of signalling intermediates downstream of the BCR revealed a perturbation of MAPK signalling pathways in p85alpha null and p110delta null B cells , and our data suggests that cross talk exists between the PI3K and JNK pathways . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Upon BCR cross linking , LIME was tyrosine phosphorylated by Lyn and associated with Lyn , Grb 2 , PLC gamma 2 , and PI3K . ^^^ Reduction of LIME expression by the introduction of siRNA resulted in the disruption of BCR mediated activation of MAPK , calcium flux , NF AT , PI3K , and NF kappaB . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
V 3 21 cases showed characteristic expression differences compared to VH MUT ( up : ZAP 70 [ or ZAP 70 ] ; down : CCND 2 , P 27 ) and VH UM ( down : PI3K , CCND 2 , P 27 , CDK 4 , BAX ) involving several BCR related genes . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
During B cell receptor ( BCR ) signaling , phosphoinositide 3 kinase ( PI3K ) is thought to function upstream of phospholipase Cgamma 2 ( PLCgamma 2 ) . ^^^ Interestingly , PLCgamma 2 deficiency had no effect on BCR mediated PI3K activation , whereas PI3K deficiency only partially blocked activation of PLCgamma 2 . ^^^ Consistent with this finding , BCR signaling was more severely impaired in the absence of both PI3K and PLCgamma 2 genes than in the absence of either one alone . ^^^ Taken together , these results demonstrate that whereas PI3K functions upstream of PLCgamma 2 , activation of PLCgamma 2 can occur independently of PI3K and that PI3K and PLCgamma 2 also have distinct functions in BCR signal transduction . . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Differential requirements of PI3K subunits for BCR or BCR / CD19 induced ERK activation . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Here , we show that BCR signaling in Y 112 LMP2A expressing cells is attenuated with a reduction in both the degree and duration of phosphorylation of key components of the BCR signaling cascade including Syk , BLNK , PI3K , and Btk . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
The use of specific ODNs or antisense constructs to downregulate p 85 alpha expression showed a requirement for p 85 alpha subunit in the proliferation of BCR / ABL dependent cell lines and chronic myelogenous leukemia ( CML ) primary cells . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
In this study , we show in both BCR ABL cells ( Mo7e p 210 and BaF / 3 p 210 ) and primary CML CD34+ cells that STI 571 inhibition of BCR ABL tyrosine kinase activity results in a G ( 1 ) cell cycle arrest mediated by the PI3K pathway . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Here , we demonstrate that IM treatment activated the phosphatidylinositol 3 kinase ( PI3K ) / Akt / mammalian target of rapamycin ( mTor ) pathway in BCR / ABL positive LAMA cells and primary leukemia cells in vitro , as well as in a chronic phase CML patient in vivo . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
Several agents interfering with intracellular targets that are components of key oncogenic signaling pathways , such as RAF kinase , phosphatidylinositol 3 kinase ( PI3K ) / Akt or Src , are in preclinical and early clinical development . `` Addictive ' ' targets , such as the Bcr Abl fusion protein in chronic myeloid leukemia ( CML ) , are critical for maintaining the malignant phenotype and hence represent an Achilles ' heel for selective drugs . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
BCR induced glucose utilization is dependent upon phosphatidylinositol 3 kinase ( PI 3K ) activity as evidenced by inhibition of glucose uptake and glycolysis with LY 294002 treatment of normal B cells and impaired glucose utilization in B cells deficient in the PI 3K regulatory subunit p85alpha . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
We show that a signaling protein , phosphatidylinositol 3 kinase ( PI 3k ) , is essential for growth of CML cells , but not of normal hematopoietic cells , and that p85alpha subunit of PI 3k co immunoprecipitates with BCR / ABL . ^^^
Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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Interacting proteins: Q13746 and P27986	Pubmed	SVM Score :0.0
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