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EPHB2 — IRS2

Text-mined interactions from Literome

Kurihara et al., Endocr J 2000 (Neuroblastoma) : PD98059 inhibited activation of Erk and LY294002 repressed activation of Akt in response to IGF-I, but did not affect tyrosine phosphorylation of the IGF-IR, IRS-1, IRS-2 , or Shc
Rui et al., J Biol Chem 2001 (Carcinoma, Hepatocellular...) : Chronic insulin or IGF-1 treatment of IRS-1-deficient mouse embryo fibroblasts inhibited IRS-2 mediated activation of Akt and ERK1/2 , which was reversed by lactacystin pretreatment
Huang et al., J Biol Chem 2005 : We conclude that insulin stimulated Akt1 phosphorylation, actin remodeling, GLUT4 translocation, and glucose uptake are regulated mainly by IRS-1, whereas IRS-2 contributes selectively to ERK signaling, and Akt2 and p38MAPK lie downstream of both IRS in muscle cells
Sugano et al., J Neurochem 2006 : The increase in IRS-1/IRS-2 levels induced by nicotine was prevented by nicotinic acetylcholine receptor ( nAChR ) antagonists, the Ca ( 2+ ) chelator 1,2-bis ( 2-aminophenoxy ) -ethane-N, N,N ', N'-tetra-acetic acid tetrakis-acetoxymethyl ester, cycloheximide or actinomycin D. Nicotine increased IRS-1 and IRS-2 mRNA levels by approximately 57 and approximately 50 %, and this was prevented by conventional protein kinase C ( cPKC ) inhibitor Gö6976, or ERK kinase inhibitors PD98059 and U0126
Niessen et al., Exp Cell Res 2007 : Overexpression of IRS1 and IRS2 inhibited insulin stimulated activation of the MAP kinases Erk1/2 while it increased/induced activation of Akt/PKB
Fulzele et al., J Biol Chem 2007 : In DeltaIGF-1R osteoblasts, insulin signaling was markedly increased as evidenced by increased phosphorylation of insulin receptor substrate 1/2 and enhanced ERK/Akt activation
Perrini et al., Endocrinology 2008 (Osteoporosis) : Augmentation of basal IGF-I receptor phosphorylation was associated with coordinate increases in basal tyrosine phosphorylation of insulin receptor substrate (IRS)-2 and activation of Erk , which were also minimally responsive to IGF-I stimulation
Wang et al., Mol Cancer Res 2010 (Breast Neoplasms...) : Sustained JNK activity enhanced insulin receptor substrate-2 mediated ERK activation, which in turn increased c-Fos expression and activator protein activity