Gene interactions and pathways from curated databases and text-mining

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CBL — PIK3R1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Take et al., Biochem Biophys Res Commun 2000 : Our results suggest that CIN85 may play a specific role in the EGF receptor mediated signaling cascade via its interaction with c-Cbl
Fang et al., Nat Immunol 2001 : Proteolysis independent regulation of PI3K by Cbl-b mediated ubiquitination in T cells
Petrelli et al., Nature 2002 : Cbl, in turn, binds and ubiquitinates activated HGF receptor , and by recruiting the endophilin-CIN85 complex , it regulates receptor internalization
Qin et al., Biochemistry 2003 : Under our conditions, hydrogen peroxide induced PI3K and Akt activation was independent of Lyn, Syk, Cbl , BCAP, or Ras when each was eliminated individually either by mutation or by a specific inhibitor
Kowanetz et al., J Biol Chem 2003 : Identification of a novel proline-arginine motif involved in CIN85 dependent clustering of Cbl and down-regulation of epidermal growth factor receptors
Guenou et al., Am J Pathol 2006 (Acrocephalosyndactylia) : Down-regulation of ubiquitin ligase Cbl induced by twist haploinsufficiency in Saethre-Chotzen syndrome results in increased PI3K/Akt signaling and osteoblast proliferation ... This provides genetic and biochemical evidence for a role for Cbl mediated PI3K signaling in the altered osteoblast phenotype induced by Twist haploinsufficiency in SCS
Peruzzi et al., J Immunol 2007 (Calcium Signaling) : We found that CIN85 overexpression inhibits the FcepsilonRI induced tyrosine phosphorylation of phospholipase Cgamma , thus altering calcium mobilization ... Altogether, our findings support a new role for CIN85 in regulating Syk protein levels in RBL-2H3 cells through the activation of the ubiquitin-proteasome pathway and provide a mechanism for this regulation involving c-Cbl ligase activity
Dufour et al., Bone 2008 : Biochemical and molecular analyses revealed that the attenuated PI3K signaling induced by FGFR2 activation is due to increased Cbl-PI3K molecular interaction mediated by the Cbl Y731 residue, which results in increased PI3K ubiquitination and proteasome degradation
Wakasaki et al., Neoplasia (New York, N.Y.) 2010 (Carcinoma, Squamous Cell...) : Little is known, however, about a role of CIN85 in EGFR signaling as well as its relevance to tumor development and progression of HNSCC
Yingchun et al., Braz J Med Biol Res 2011 : In the present study, we evaluated whether E3 ubiquitin ligase Cbl-b , a negative regulator of PI3K activation, is involved in the action of ATO
Marois et al., J Biol Chem 2011 : Silencing the expression of CIN85 by siRNA in dibutyryl cyclic AMP differentiated PLB 985 cells prevented Fc?RIIa degradation and increased IgG mediated phagocytosis
Sévère et al., J Biol Chem 2011 : Analysis of molecular mechanisms revealed that the Cbl mutant increased PDGF receptor a and FGF receptor 2 but not EGF receptor expression in hMSCs, resulting in increased ERK1/2 and PI3K signaling
Tossidou et al., Mol Cell Biol 2012 : Our results indicate a novel role for CD2AP in regulating posttranslational modification of CIN85
Guo et al., Cell reports 2012 : Here, we report that Cbl-b does not inhibit PI3K but rather suppresses TCR/CD28 induced inactivation of Pten
Samoylenko et al., Carcinogenesis 2012 (Adenocarcinoma...) : Thereby, Ruk ( l ) /CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src , Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility ... Thereby, Ruk ( l ) /CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src, Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility ... Thereby, Ruk ( l ) /CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src, Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility
Schroeder et al., Mol Biol Cell 2012 : In this study we show that EGFR activation leads to a pronounced src mediated tyrosine phosphorylation of CIN85 that subsequently influences EGFR ubiquitination
Bior et al., FEBS Lett 2013 : Dab1 stabilizes its interaction with Cin85 by suppressing Cin85 phosphorylation at serine 587 ... Furthermore a Cin85 Ser587 phosphomimetic disrupts the Dab1-Cin85 complex without affecting the Cin85-CapZ complex
Fuchigami et al., Genes Cells 2013 : We reported previously that Cdk5-p35 phosphorylates Dab1 at Ser400 and Ser491 and the phosphorylation regulates its binding to CIN85 , which is an SH3 containing multiadaptor protein involved in endocytic downregulation of receptor-tyrosine kinases ... We reported previously that Cdk5-p35 phosphorylates Dab1 at Ser400 and Ser491 and the phosphorylation regulates its binding to CIN85 , which is an SH3 containing multiadaptor protein involved in endocytic downregulation of receptor-tyrosine kinases ... We reported previously that Cdk5-p35 phosphorylates Dab1 at Ser400 and Ser491 and the phosphorylation regulates its binding to CIN85 , which is an SH3 containing multiadaptor protein involved in endocytic downregulation of receptor-tyrosine kinases
Saci et al., J Biol Chem 1999 : Our results suggest that Cbl is involved in platelet signal transduction by the recruitment of PI 3-K to the FcgammaRIIa pathway, possibly by increasing PI 3-K activity