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EGF — IRS1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: IRS1 → EGF (increases) Olsen et al., Cell 2006*
  Evidence: We have detected 6,600 phosphorylation sites on 2,244 proteins and have determined their temporal dynamics after stimulating HeLa cells with epidermal growth factor (EGF) and recorded them in the Phosida database
• OpenBEL Selventa BEL large corpus: IRS1 → EGF (increases) Gogg et al., J Biol Chem 2002*
  Evidence: EGF increased the tyrosine phosphorylation of several proteins (the EGF receptor,insulin receptor substrate (IRS)-1, IRS-2, and Grb2-associated binder 1)
• OpenBEL Selventa BEL large corpus: IRS1 → EGF (increases) Fantin et al., J Biol Chem 1998
  Evidence: epidermal growth factor and interleukin-4 elicit tyrosine phosphorylation of IRS1

Text-mined interactions from Literome

Lingohr et al., Diabetes 2002 (MAP Kinase Signaling System) : Neither IRS-1 nor IRS-2 overexpression induced a beta-cell proliferative response to TGF-alpha/EGF
Gogg et al., J Biol Chem 2002 (Insulin Resistance) : EGF increased the tyrosine phosphorylation of several proteins ( the EGF receptor, insulin receptor substrate (IRS)-1 , IRS-2, and Grb2 associated binder 1 ), whereas Shc and Gab2 were only weakly and inconsistently phosphorylated ... Both insulin and EGF increase the tyrosine phosphorylation and activation of IRS-1 and IRS-2, whereas EGF is also capable of activating additional PI 3-kinase pools and, thus, can augment the downstream signaling of insulin in insulin-resistant states like Type 2 diabetes
Hardy et al., Endocrinology 1995 : EGF did not stimulate tyrosine phosphorylation of the insulin receptor or insulin receptor substrate-1
Burgaud et al., Exp Cell Res 1996 (Cell Transformation, Viral) : The mutant IGF-I receptors are activated ( tyrosyl phosphorylation of IRS-I ) in response to EGF