Gene interactions and pathways from curated databases and text-mining

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IGF1 — SRC

Pathways - manually collected, often from reviews:

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
Gruden et al., Kidney Int 2003 : IGF-I induces vascular endothelial growth factor in human mesangial cells via a Src dependent mechanism ... IGF-I induces VEGF gene expression and protein secretion in human mesangial cells via a Src dependent mechanism
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 ... 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 ... These results suggest that the loss of IGF-I downstream mitogenic signaling in differentiating 3T3-L1 cells is due to a change in IGF-I activation of c-Src and CSK may mediate the inactivation of c-Src by IGF-I in 3T3-L1 adipogenesis
Sekimoto et al., Mol Endocrinol 2005 : ( alpha ) v ( beta ) 3 integrins and Pyk2 mediate insulin-like growth factor I activation of Src and mitogen activated protein kinase in 3T3-L1 cells ... IGF-I increased tyrosine phosphorylation of the focal adhesion kinase ( FAK ) Pyk2 ( calcium dependent proline-rich tyrosine kinase-2 ) to a much greater extent than FAK, and increased association of Src with Pyk2 but not FAK
Knowlden et al., Endocrinology 2005 (Breast Neoplasms) : 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
Lieskovska et al., J Biol Chem 2006 (MAP Kinase Signaling System) : IGF-I induced both Src/SHP-2 and Src/SHPS-1 association ... IGF-I induced association of Src and SHPS-1 was also impaired in SHP-2Delata10 expressing cells, although SHP-2/SHPS-1 association was unaffected
Fleming et al., Endocrinology 2006 : Interestingly, inhibition of Src activation blocked the ability of EGF, but not IGF-I , to activate AKT
Meng et al., Free Radic Biol Med 2007 : IGF-I stimulated ROS production and Src activation
Di et al., Hum Reprod 2008 (Leiomyoma...) : Additionally, extracellular regulated kinase (ERK), Src homology/collagen (Shc) and ER alpha were transiently activated, and interactions between ER alpha and IGF-I receptor (IGF-IR) were rapidly induced by genistein in LM cells
Xi et al., J Biol Chem 2010 : These studies were conducted to determine how p66 ( shc ) alters IGF-I stimulated Src activation, leading to decreased IGF-I actions ... Disruption of this interaction using a synthetic peptide containing the p66 ( shc ) polyproline domain or expression of a p66 ( shc ) mutant containing substitutions for the proline residues ( P47A/P48A/P50A ) resulted in enhanced Src kinase activity, p52 ( shc ) phosphorylation, MAPK activation, and cell proliferation in response to IGF-I
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 ... Pyk2 recruitment to SHPS-1 is mediated via the interaction of Pyk2 Tyr402 and the Src in response to IGF-I
Shen et al., J Biol Chem 2010 : A proline-rich sequence in PDK1 bound to an Src homology 3 domain in Grb2 in response to IGF-I
Xi et al., Diabetes 2012 (Hyperglycemia) : Hyperglycemia enhances IGF-I stimulated Src activation via increasing Nox4 derived reactive oxygen species in a PKC? dependent manner in vascular smooth muscle cells ... IGF-I stimulated sarcoma viral oncogene (Src) activation during hyperglycemia is required for propagating downstream signaling ... The aim of the current study was to determine the mechanism by which hyperglycemia enhances IGF-I stimulated Src activation and the role of NADPH oxidase 4 (Nox4) and protein kinase C ? ( PKC? ) in mediating this response in vascular smooth muscle cells ( VSMCs ) ... The role of Nox4 derived reactive oxygen species ( ROS ) in IGF-I stimulated Src activation was investigated via knockdown of Nox4 ... Knockdown of Nox4 prevented ROS generation and impaired the oxidation and activation of Src in response to IGF-I , whereas knockdown of Nox1 had no effect ... Nox4 derived ROS is responsible for the enhancing effect of hyperglycemia on IGF-I stimulated Src activation, which in turn amplifies IGF-I linked downstream signaling and biological actions
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
Xi et al., J Biol Chem 2013 (Diabetes Mellitus, Experimental) : Recruitment of Nox4 to a plasma membrane scaffold is required for localized reactive oxygen species generation and sustained Src activation in response to insulin-like growth factor-I ... Nox4 derived ROS is increased in response to hyperglycemia and is required for IGF-I stimulated Src activation ... IGF-I stimulated sustained Src activation, which occurred primarily on the SHPS-1 scaffold protein