◀ Back to PIK3CA
BCR — PIK3CA
Pathways - manually collected, often from reviews:
-
Reactome Reaction:
BCR
→
PIK3CA
(indirect_complex)
Guasch et al., Mol Cell Biol 2001, Demiroglu et al., Blood 2001, Chen et al., Proc Natl Acad Sci U S A 2004, Jackson et al., Hum Pathol 2010
-
Reactome Reaction:
BCR
→
PIK3CA
(reaction)
Guasch et al., Mol Cell Biol 2001, Demiroglu et al., Blood 2001, Chen et al., Proc Natl Acad Sci U S A 2004, Jackson et al., Hum Pathol 2010
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
Ramadani et al., Science signaling 2010
:
Unlike p110delta, however,
p110alpha did not
contribute to agonist induced
BCR signaling
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