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CD79A — PIK3R1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database BCR signaling pathway:
B-cell antigen/BCR complex/LYN/SYK complex (LYN-SYK-CD79B-CD79A)
→
PI3K/BCAP/CD19 complex (CD19-PIK3CA-PIK3R1)
(modification, activates)
Okada et al., Immunity 2000, Weng et al., J Biol Chem 1994
Evidence: assay, physical interaction
-
NCI Pathway Database BCR signaling pathway:
B-cell antigen/BCR complex/LYN/SYK complex (LYN-SYK-CD79B-CD79A)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Okada et al., Immunity 2000, Weng et al., J Biol Chem 1994
Evidence: assay, physical interaction
-
NCI Pathway Database BCR signaling pathway:
B-cell antigen/BCR complex/LYN complex (LYN-CD79B-CD79A)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Marshall et al., J Exp Med 2000, Anderson et al., Curr Biol 2000
Evidence: assay, physical interaction
Text-mined interactions from Literome
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
Bracke et al., J Leukoc Biol 2000
(Asthma...) :
Moreover, inhibition of
PI3K in these cells
blocked the background and the TNF-alpha induced
IgA binding completely
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
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
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
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
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