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CTLA4 — PIK3R1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Hprd Interaction:
CTLA4
—
PIK3R1
(in vitro)
Schneider et al., J Exp Med 1995*
-
IRef Hprd Interaction:
CTLA4
—
PIK3R1
(in vivo)
Schneider et al., J Exp Med 1995*
-
IRef Intact Interaction:
CTLA4
—
PIK3R1
(association, pull down)
Bradshaw et al., Biochemistry 1997*
-
IRef Intact Interaction:
CTLA4
—
PIK3R1
(association, coimmunoprecipitation)
Schneider et al., J Exp Med 1995*
-
IRef Intact Interaction:
CTLA4
—
PIK3R1
(association, coimmunoprecipitation)
Schneider et al., Biochem Biophys Res Commun 1998*
-
IRef Ophid Interaction:
CTLA4
—
PIK3R1
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Parry et al., Mol Cell Biol 2005
:
Lastly, PD-1 ligation is more effective in suppressing CD3/CD28 induced changes in the T-cell transcriptional profile, suggesting that differential
regulation of
PI3K activation by PD-1 and
CTLA-4 ligation results in distinct cellular phenotypes
Schneider et al., PloS one 2008
:
CTLA-4 ligation
induced PI 3K activation as evidenced by the phosphorylation of PKB/AKT that in turn inactivated GSK-3 ...
CTLA-4 induced
PI 3K and AKT activation also led to phosphorylation of the pro-apoptotic factor BAD as well as the up-regulation of BcL-XL
Rudd et al., Immunol Rev 2009
:
We also present recent findings on T-cell receptor interacting molecule ( TRIM ) regulation of CTLA-4 surface expression, and a signaling pathway involving
CTLA-4 activation of
PI3K and protein kinase B (PKB)/AKT by which cell survival is ensured under conditions of anergy induction