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IGF2 — SRC

Text-mined interactions from Literome

Arbet-Engels et al., J Biol Chem 1999 : The results suggest that c-Src and CSK are involved in IGF-IR and IR signaling and that the interaction of CSK with the IGF-IR may play a role in the decrease in c-Src activity following IGF-I stimulation
Tanno et al., Cancer Res 2001 (Neoplasm Invasiveness...) : Furthermore, AKT induced IGF-IR expression was down-regulated by dominant negative Src or PTEN
Sumitomo et al., Cancer Res 2001 (Prostatic Neoplasms) : Incubation of TSU-Pr1 cells with specific kinase inhibitors together with ET-1 or bombesin showed that IGF-IR activation is required for neuropeptide induced Akt phosphorylation, and that neuropeptide induced Akt activation is predominantly mediated by Src and phosphatidylinositol 3-kinase but not by mitogen activated protein kinase or protein kinase C
Hallak et al., Hepatology 2002 : EGF stimulated the tyrosine phosphorylation of Src , and induced its association with the IGF-IR
Zeng et al., Biochem Biophys Res Commun 2003 (Neoplasm Invasiveness...) : On the other hand Src activation through IGF-IR is required for the cell proliferation, invasion, and also VPF/VEGF expression
Sekimoto et al., Endocrinology 2003 : Src activity increased 2- to 4-fold in IGF-I stimulated proliferating cells ; however, IGF-I had a marginal affect on Src activity in growth arrested cells and inhibited Src activity localized at the membrane in differentiating cells
Kim et al., J Invest Dermatol 2004 (MAP Kinase Signaling System) : These results suggest that IGF-II induces COX-2 expression through the tyrosine kinase-Src-ERK and tyrosine kinase-PI3-kinase pathways, but not via p38 MAPK pathway, and that the basal JNK activity is required for the upregulation of COX-2 by IGF-II, as well
Knowlden et al., Endocrinology 2005 (Breast Neoplasms) : IGF-II promoted direct association of c-SRC with IGF-IR, phosphorylated c-SRC , and increased EGFR phosphorylation at tyrosine 845, a c-SRC dependent phosphorylation site ... The c-SRC inhibitor SU6656 also inhibited growth, reduced basal and IGF-II induced c-SRC and EGFR phosphorylation, and blocked EGFR activation by TGFalpha ... Similarly, in T47D-R cells, AG1024 and SU6656 inhibited basal and IGF-II induced phosphorylation of c-SRC and EGFR, and SU6656 reduced TGFalpha induced EGFR activity ... These results suggest the existence of a unidirectional IGF-IR/EGFR cross-talk mechanism whereby IGF-II, acting through the IGF-IR, regulates basal and ligand activated EGFR signaling and cell proliferation in a c-SRC dependent manner in Tam-R cells ... These results suggest the existence of a unidirectional IGF-IR/EGFR cross-talk mechanism whereby IGF-II , acting through the IGF-IR, regulates basal and ligand activated EGFR signaling and cell proliferation in a c-SRC dependent manner in Tam-R cells
Carver et al., J Biol Chem 2010 (Breast Neoplasms) : Src family kinase activity was required for IGF-IR association with SHP-2, ligand induced IGF-IR internalization, and PRL enhanced IGF-IR phosphorylation
Shen et al., Cell Mol Life Sci 2010 (MAP Kinase Signaling System) : In vascular smooth muscle cells, IGF-I stimulates SHPS-1/SHP2/Src complex formation which is required for IGF-I stimulated cell proliferation
Trerotola et al., J Cell Physiol 2012 (Prostatic Neoplasms) : These enhanced Src and FAK activities are not mediated by changes in either the activity of IGF-IR , which is known to bind RACK1, or IGF-IR 's ability to associate with ß ( 1 ) integrins
Fujita et al., J Biol Chem 2013 : Inhibitors of IGF1R, Src , AKT, and ERK1/2 did not suppress avß3-IGF-IGF1R ternary complex formation, suggesting that activation of these kinases are not required for ternary complex formation