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IRS1 — POLDIP2

Text-mined interactions from Literome

Garrouste et al., Cell Death Differ 2002 : In this model, IGF-I did not activate the focal adhesion kinase, whereas it induced tyrosine phosphorylation of the insulin receptor substrate-1 and activation of the extracellular signal related kinase 1 and 2, p38 , phosphatidylinositol 3'-kinase and protein kinase B/Akt
Hers et al., Biochem J 2005 : Furthermore, inhibition of mTOR/p70S6 kinase, JNK or p38MAPK had no effect on insulin stimulated IRS-1 tyrosine phosphorylation
Carlson et al., Metabolism 2005 (Insulin Resistance) : However, p38 inhibition did not prevent the loss of IRS-1 protein levels or insulin signaling to PKB in insulin-resistant cells
Hemi et al., Diabetes 2011 (Insulin Resistance) : Liver expression of dominant negative ( DN ) -p38MAPKa in ob/ob mice reduced fasting insulin levels and improved glucose tolerance, whereas C57/BL6 mice overexpressing wild-type p38MAPKa exhibited enhanced IRS-1 serine phosphorylation and reduced insulin stimulated IRS-1 tyrosine phosphorylation