◀ Back to INS

INS — MAP2K1

Text-mined interactions from Literome

Benes et al., Biochem J 1999 : We found that this transcription is regulated in the MIN6 cells in the same range of glucose concentration as in primary islets, and that specific inhibition of mitogen activated protein kinase kinase , the direct activator of ERK, impaired the response of the insulin gene to glucose
Fujishiro et al., Mol Endocrinol 2003 (Insulin Resistance) : The MEK1 mutant, which activates ERK, markedly down-regulated expression of the insulin receptor (IR) and its major substrates, IRS-1 and IRS-2, mRNA and protein, and in turn reduced tyrosine phosphorylation of IR as well as IRS-1 and IRS-2 and their associated phosphatidyl inositol 3-kinase (PI3K) activity
Xu et al., J Biol Chem 2006 : Insulin restored the ability of a second GH exposure to induce phosphorylation of MEK1/2 and ERK1/2 without altering GH receptor levels or GH-induced phosphorylation/activation of JAK2 and Raf-1
Kawakami et al., Circulation 2008 (Disease Models, Animal...) : The impaired insulin signaling was restored by PKCbeta inhibitor or MEK1 inhibitor
Gao et al., J Appl Physiol 2008 : Addition of insulin to proteolytically active cells attenuated both responses within 4 h. Individually, inhibitors of either phosphatidylinositide 3-kinase (PI3K) or MEK1/2 partially blocked the insulin induced reduction in caspase-3 activity ; in combination, the inhibitors completely prevented insulin from attenuating caspase-3 activity
Lim et al., Endocrinology 2009 : Knockdown or inhibition of Cdc42 and PAK1 activities also prevented activation of MAPK/ERK (MEK)-1/2-ERK1/2 by insulin , which was previously identified as a critical pathway for insulin regulated GLP-1 release
Ueki et al., J Biol Chem 1994 : Feedback regulation of mitogen activated protein kinase kinase kinase activity of c-Raf-1 by insulin and phorbol ester stimulation
Carel et al., Endocrinology 1996 : Reduced phosphorylation of mitogen activated protein kinase kinase in response to insulin in cells with truncated C-terminal domain of insulin receptor
Calleja et al., Endocrinology 1997 : Thus, in NIH3T3 fibroblasts expressing NGF receptors ( NIH3T3/trk cells ) we found that cAMP potentiates NGF stimulated ERK1 and MEK1 activities, whereas in NIH3T3 fibroblasts expressing insulin receptors ( NIH3T3/IR cells ) we saw no effect of cAMP on the activation of insulin stimulated ERK1 and MEK1
Kim et al., Biochem J 1997 : Insulin regulation of mitogen activated protein kinase kinase ( MEK ), mitogen activated protein kinase and casein kinase in the cell nucleus : a possible role in the regulation of gene expression
Carlsen et al., Cell Signal 1997 : Insulin stimulated glycogen synthesis was inhibited by the phosphatidylinositol 3-kinase inhibitors wortmannin ( IC50 approximately 40 nM ) and LY 294002 ( IC50 approximately 20 microM ) and the mitogen activated protein kinase kinase inhibitor PD 98059 ( IC50 approximately 40 microM )
Antoine et al., Endocrinology 1998 : Insulin induction of protein kinase C alpha expression is independent of insulin receptor Tyr1162/1163 residues and involves mitogen activated protein kinase kinase 1 and sustained activation of nuclear p44MAPK