Gene interactions and pathways from curated databases and text-mining

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CBL — PI3

Text-mined interactions from Literome

Hakak et al., Oncogene 2000 : Activation of PI3-kinase by v-Src may be mediated by the association of the adapter protein Cbl with the p85 subunit
Saci et al., Biochem J 2000 : The results show that, following integrin alpha IIb-beta 3 engagement, Cbl is tyrosine phosphorylated, recruits PI 3-kinase to this integrin signalling pathway and possibly enhances PI 3-kinase activity, downstream of Src-family tyrosine kinases and Syk activation
Miao et al., Biochem Biophys Res Commun 2002 : Our results suggest that Cbl plays a critical role in the shear stress induction of PI 3-kinase and JNK activities, and that this shear induced activation requires the interaction of endothelial integrins with extracellular matrix proteins
Miura et al., Biochemistry 2003 : The thiazolidinedione ( TZD ), rosiglitazone, has previously been found to tyrosine-phosphorylate Cbl and activate Cbl dependent phosphatidylinositol (PI) 3-kinase and atypical protein kinase Cs ( aPKCs ) while stimulating glucose transport in 3T3/L1 adipocytes ... These mutants diminished the interaction of Cbl with the p85 subunit of PI 3-kinase and inhibited subsequent increases in Cbl dependent PI 3-kinase activity, aPKC activity, and glucose transport
Standaert et al., Biochemistry 2004 : Cbl , via pYXXM motifs at tyrosine-371 and tyrosine-731, also activates phosphatidylinositol (PI) 3-kinase , which is required to activate atypical protein kinase C ( aPKC ) and glucose transport during thiazolidinedione action in 3T3/L1 and human adipocytes [ Miura et al. ( 2003 ) Biochemistry 42, 14335-14341 ] ... Interestingly, these mutants inhibited insulin induced increases in ( a ) binding of Cbl to both Crk and the p85 subunit of PI 3-kinase, ( b ) activation of Cbl dependent PI 3-kinase , ( c ) activation and translocation of aPKC to the plasma membrane, ( d ) translocation of Glut4 to the plasma membrane, ( e ) and glucose transport ... In contrast to Cbl dependent PI 3-kinase, Cbl mutants did not significantly inhibit the activation of PI 3-kinase by IRS-1, which is also required during insulin action
Lottin-Divoux et al., Cell Signal 2006 (Lymphoma) : First, CD21 activation triggered Cbl tyrosine phosphorylation, which required c-Src kinase but not PI 3-kinase or Syk kinase activities
Molero et al., Diabetes 2006 (Thinness) : These results indicate that c-Cbl ubiquitin ligase activity, but not c-Cbl dependent activation of PI 3-kinase , plays a key role in the regulation of whole-body energy metabolism
Cerboni et al., Eur J Immunol 1998 : CD16 mediated activation of phosphatidylinositol-3 kinase (PI-3K) in human NK cells involves tyrosine phosphorylation of Cbl and its association with Grb2, Shc, pp36 and p85 PI-3K subunit
Zell et al., Curr Biol 1998 : Mutations of the CD28 cytoplasmic domain that blocked integrin activation also impaired the tyrosine phosphorylation of the Cbl adaptor protein and the activation of the PI 3-kinase that was associated with Cbl