Gene interactions and pathways from curated databases and text-mining

◀ Back to MAPK14

IRS1 — MAPK14

Text-mined interactions from Literome

Inoue et al., Diabetologia 1999 : Variables of the IGF-1 signalling pathway, including tyrosine phosphorylation of insulin receptor substrate-1 and activation of mitogen activated protein kinase and phosphatidyl inositol 3 kinase, were also augmented in mutant cells
Uchida et al., Mol Cell Biol 2000 : Insulin promoted the association of Grb-2 with IRS-1 and IRS-4, whereas IRS-2 weakly bound Grb-2 ; consequently, IRS-1 and IRS-4 enhanced insulin stimulated mitogen activated protein kinase activity
Formisano et al., Mol Cell Biol 2000 (MAP Kinase Signaling System) : In L6hIR cells, inhibition of insulin receptor substrate 1 (IRS-1) expression caused a 90 % decrease in insulin induced PKCalpha and -beta activation and blocked insulin stimulation of mitogen activated protein kinase ( MAPK ) and DNA synthesis
Liang et al., Endocrinology 2000 : Insulin receptor substrate-1 mediated enhancement of growth hormone induced mitogen activated protein kinase activation
Weng et al., Hum Mol Genet 2001 (Breast Neoplasms) : PTEN inhibits insulin stimulated MEK/MAPK activation and cell growth by blocking IRS-1 phosphorylation and IRS-1/Grb-2/Sos complex formation in a breast cancer model
Pirola et al., J Biol Chem 2003 (MAP Kinase Signaling System) : PDK1, mTOR, and MAPK inhibitors did not block insulin induced reduction of IRS-1 , suggesting that the PI3K serine-kinase activity causes IRS-1 serine phosphorylation and its commitment to proteasomal degradation
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
Lim et al., Diabetologia 2006 : We show distinct mitochondrial retrograde signalling, where Irs1 is downregulated through ATF3 in a Ca ( 2+ ) -, JNK- and p38 MAPK dependent manner, and IRS1 is inactivated
Bergman et al., Diabetes 2012 (Insulin Resistance) : Inhibition of mTOR, but not p44/42 MAPK , during nicotine exposure prevented IRS-1 ( ser636 ) phosphorylation and normalized insulin sensitivity
Taha et al., J Biol Chem 1995 : Insulin binding results in rapid phosphorylation of insulin receptor substrate-1 to activate p21ras and mitogen activated protein kinase
Mèndez et al., Mol Cell Biol 1996 : Expression of more IR permits partial stimulation of mitogen activated protein kinase by insulin, and expression of IRS-1 alone mediates insulin stimulation of the 70-kDa S6 kinase ( pp70S6K ) by the endogenous IR
Sharma et al., Mol Cell Biol 1997 : Thus, interference with the IRS-1-IR interaction inhibits insulin stimulated IRS-1 and Shc phosphorylation, PI 3-K enzymatic activity, p70s6k activation, MAPK phosphorylation and cell cycle progression
De Fea et al., J Biol Chem 1997 : In the present studies we have examined the potential role of the mitogen activated protein ( MAP ) kinase in the increased serine phosphorylation of IRS-1 observed in human embryonic kidney cells treated with an activator of protein kinase C, phorbol 12-myristate 13-acetate