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INSR — MAPK3

Pathways - manually collected, often from reviews:

• KEGG Type II diabetes mellitus: INSR → MAPK1/MAPK3 (protein-protein, indirect effect)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: MAPK3 — INSR (physical association, affinity chromatography technology) Lin et al., Mol Cell Biol Res Commun 2000*
• IRef Hprd Interaction: MAPK3 — INSR (in vivo) Lin et al., Mol Cell Biol Res Commun 2000*
• IRef Innatedb Interaction: Complex of INSR-MAPK1-MAPK3 (unknown, -) Lin et al., Mol Cell Biol Res Commun 2000*
• IRef Ophid Interaction: MAPK3 — INSR (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Martínez de Ubago et al., Biochim Biophys Acta 2009 (Carcinoma, Hepatocellular...) : OEA dose-dependently activates JNK and p38 MAPK , and inhibits insulin receptor phosphorylation
Cazarolli et al., Eur J Pharmacol 2013 : The presence of specific insulin signaling inhibitors, such as wortmannin, an inhibitor of phosphoinositide 3-kinase (PI3K), RO318220, an inhibitor of protein kinase C ( PKC ), PD98059, an inhibitor of mitogen activated protein kinase ( MEK ) , HNMPA ( AM ) 3, an insulin receptor tyrosine kinase activity inhibitor , colchicine, a microtubule depolymerizing agent, SB239063, an inhibitor of P38 MAPK and cycloheximide, an inhibitor of protein synthesis showed that kaempferitrin triggers different metabolic and nuclear pathways in skeletal muscle
Chang et al., J Biol Chem 1995 : We conclude that ( i ) transgenic expression of kinase-defective insulin receptors exerts dominant negative effects at the level of receptor auto-phosphorylation and kinase activation ; ( ii ) insulin receptor tyrosine kinase activity is required for in vivo insulin stimulated IRS-1 phosphorylation, IRS-1 associated PI 3-kinase activation, phosphorylation of mitogen activated protein kinase , and c-fos gene induction in skeletal muscle ; ( iii ) hybrid receptor formation is likely to contribute to the in vivo dominant negative effects of kinase-defective receptor expression
Myers et al., Mol Cell Biol 1994 : Coexpression of IRS-1 or IRS-1F-895 with the insulin receptor was required for insulin stimulated mitogenesis in 32-D cells, while expression of the insulin receptor alone was sufficient to mediate insulin stimulated tyrosine phosphorylation of Shc and activation of p21ras and mitogen activated protein ( MAP ) kinase