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EGF — IRS2

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: IRS2 → 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

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
Cui et al., Cancer Res 2006 (Breast Neoplasms) : Although both extracellular signal regulated kinase and c-Jun NH ( 2 ) -terminal kinase ( JNK ) signaling pathways were involved in the EGF up-regulation of IRS-1, the IRS-2 induction by EGF was specifically mediated by JNK signaling ... Consistent with this, EGF increased IRS-2 promoter activity, which was associated with recruitment of activator protein-1 (AP-1) transcription factors and was inhibited by blocking AP-1 activity ... Finally, repressing the induction of IRS-2 levels abolished the EGF enhancement of cell motility, suggesting that increased IRS-2 is essential for the EGF regulation of breast cancer cell migration