Gene interactions and pathways from curated databases and text-mining

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BCR — PIK3R1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Beitz et al., J Biol Chem 1999 : Whereas CD19 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 p85 PI3K
Otero et al., J Biol Chem 2001 (Lymphoma, B-Cell) : A prominent feature of CD19 signaling is the binding and activation of phosphoinositide 3-kinase ( P13K ), which accounts for the majority of PI3K activity induced by BCR ligation
Ingham et al., J Biol Chem 2001 : Moreover, using confocal microscopy, we show that BCR ligation can induce the translocation of Gab1 from the cytosol to the plasma membrane and that this requires the Gab1 PH domain as well as PI3K activity
Che et al., Circulation 2001 : Because phosphatidylinositol 3'-kinase (PI3-K) is essential for Bcr/Abl leukemogenesis, we evaluated the role of mouse PDGF-beta-receptor binding sites for PI3-K ( Y708, Y719 ) and for phospholipase C-gamma ( Y977, Y989 ) in PDGF mediated Bcr kinase activation
Granboulan et al., J Biol Chem 2003 : 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
Glassford et al., Eur J Immunol 2005 : 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 D2 mRNA expression via transcriptional activation of the cyclin D2 promoter and that this transcriptional activation of cyclin D2 requires PI3K activity
Ahn et al., Blood 2006 : 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
Dai et al., Mol Cell Biol 2006 : Interestingly, PLCgamma2 deficiency had no effect on BCR mediated PI3K activation, whereas PI3K deficiency only partially blocked activation of PLCgamma2
Vigorito et al., Cell Signal 2006 : We found that PKD activation upon BCR engagement or coligation of the BCR with CD19 is entirely dependent on PI3K and PLCgamma but differ in the requirement for Vav proteins
Donahue et al., Eur J Immunol 2007 : We used flow cytometry and magnetic cell sorting to examine the requirement for PI3K and mTOR in responses of splenic B cell subsets to BCR and LPS stimulation
Aiba et al., Blood 2008 : Together, our data suggest that BCAP and CD19 have complementary roles in BCR mediated PI3K activation, thereby, at least in part, contributing to B-cell development
Weisberg et al., Blood 2008 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive...) : Potentiation of antileukemic therapies by the dual PI3K/PDK-1 inhibitor, BAG956 : effects on BCR-ABL- and mutant FLT3 expressing cells
Hodson et al., Adv Exp Med Biol 2009 : Although CD40, TLR and cytokines all activate PI3K the BCR seems especially dependent upon PI3K signalling
Xu et al., Immunol Cell Biol 2012 : To understand the mechanisms of PI3K regulation during B-cell activation, we performed a series of biochemical analysis on primary B cells, and found that activity of Src family tyrosine kinases (SFK) is crucial for the activation of PI3K following BCR ligation and this is regulated by the SFK Lyn
Hanihara et al., Int Immunol 2013 : The PI3K inhibitor LY294002 inhibited BCR mediated, but not TLR mediated, induction of I?B-?, consistent with the role of PI3K in BCR signaling and its suppression by Fc?R. Analysis of I?B-?-deficient B cells demonstrated that I?B-? was essential upon stimulation of BCR or TLR for the expression of several genes including IL-10 and CTLA4
Skorski et al., Blood 1995 (Blast Crisis...) : Phosphatidylinositol-3 kinase activity is regulated by BCR/ABL and is required for the growth of Philadelphia chromosome positive cells