Gene interactions and pathways from curated databases and text-mining

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CBFA2T2 — IGF1

Text-mined interactions from Literome

Isenović et al., Metabolism 2002 : Both Iso and IGF-1 induced an increase in p85 subunit phosphorylation as demonstrated by Western analysis, effects inhibited by preincubation with WT. Iso also enhanced association of p85 with the Triton X-100-insoluble fraction of RAEC, reflecting translocation of this enzyme to a cytoskeletal fraction
Li et al., Arterioscler Thromb Vasc Biol 2003 : Moreover, a dominant negative p85 phosphatidylinositol 3-kinase adenovirus blocked the capacity of the IGF-1 receptor to prevent oxidized LDL induced apoptosis
Isenovic et al., Int J Mol Med 2004 : IGF-1 increased the association between IRS-1 and p85 , and Ang II as well as PI3K inhibition decreased this IGF-1 effect
Hers et al., Blood 2007 : IGF-1 stimulated tyrosine phosphorylation of IRS-1 and IRS-2 and subsequent p85 binding is transient and precedes phosphorylation of protein kinase B (PKB) on Ser473
Xi et al., Endocrinology 2010 (Hyperglycemia) : Mechanistic studies showed that knockdown of p66shc enhanced IGF-I stimulated SHPS-1/p85, p85/SHP-2 , and p85/Grb2 association, all of which are required for PI-3 kinase/AKT activation
Giorgino et al., J Biol Chem 1997 : Stimulation with IGF-I induced the association of p85alpha and p85beta with IRS-1, and this was accompanied by increased amounts of the p110 catalytic subunit and markedly increased PI 3-kinase activity in IRS-1 immunoprecipitates
Valverde et al., Mol Endocrinol 1998 : Insulin/IGF-I rapidly stimulated IRS-1 and IRS-2 tyrosine phosphorylation, their association with p85alpha , and IRS-1- and IRS-2 associated phosphatidylinositol (PI) 3-kinase activation to the same extent, the effect of insulin being stronger than the effect of IGF-I at the same physiological dose ( 10 nM ) ... Pull-down experiments with glutathione-S-transferase-fusion proteins containing SH2-domains of p85alpha revealed a strong association between IRS-1 and IRS-2 with p85alpha in response to insulin/IGF-I , the insulin effect being stronger than IGF-I