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CBL — PIK3CA

Pathways - manually collected, often from reviews:

• BioCarta il-2 receptor beta chain in t cell activation: CBL → PI3K complex (PIK3CA-PIK3R1) (modification, activates)
  
• KEGG Pathways in cancer: Complex of CBL-CBLB-CBLC-CRK-CRKL → PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 (protein-protein, activation)
  
• KEGG Chronic myeloid leukemia: Complex of CBL-CBLB-CBLC-CRK-CRKL → PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 (protein-protein, activation)
  
• NCI Pathway Database IL4-mediated signaling events: CBL (CBL) → PI3K complex (PIK3CA-PIK3R1) (modification, activates)
  Ueno et al., Blood 1998*
  Evidence: mutant phenotype, physical interaction
• Reactome Reaction: CBL → PIK3CA (indirect_complex) Dufour et al., Bone 2008, Odai et al., J Biol Chem 1995, Anderson et al., J Biol Chem 1997, Hunter et al., Mol Endocrinol 1997, Feshchenko et al., J Biol Chem 1998, Park et al., J Immunol 1998
• Reactome Reaction: CBL → PIK3CA (reaction) Odai et al., J Biol Chem 1995, Anderson et al., J Biol Chem 1997, Hunter et al., Mol Endocrinol 1997, Feshchenko et al., J Biol Chem 1998, Park et al., J Immunol 1998

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: CBL — PIK3CA (physical association, affinity chromatography technology) Chernock et al., Blood 2001
• IRef Biogrid Interaction: CBL — PIK3CA (physical association, affinity chromatography technology) Sattler et al., J Cell Physiol 1997*
• IRef Biogrid Interaction: CBL — PIK3CA (physical association, affinity chromatography technology) Brehme et al., Proc Natl Acad Sci U S A 2009
• IRef Intact Interaction: Complex of 13 proteins (association, tandem affinity purification) Brehme et al., Proc Natl Acad Sci U S A 2009
• IRef Intact Interaction: Complex of 12 proteins (association, tandem affinity purification) Brehme et al., Proc Natl Acad Sci U S A 2009

Text-mined interactions from Literome

Fang et al., Nat Immunol 2001 : Proteolysis independent regulation of PI3K by Cbl-b mediated ubiquitination in T cells
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
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
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
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
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
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
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