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IRS2 — SOCS1

Pathways - manually collected, often from reviews:

• KEGG Type II diabetes mellitus: SOCS1/SOCS2/SOCS3/SOCS4 → IRS1/IRS2/IRS4 (protein-protein, inhibition)

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: IRS2 — SOCS1 (physical association, affinity chromatography technology) Rui et al., J Biol Chem 2002*

Text-mined interactions from Literome

Rui et al., J Biol Chem 2002 (Insulin Resistance) : Adenoviral mediated expression of SOCS1 in mouse liver dramatically reduced hepatic IRS1 and IRS2 protein levels and caused glucose intolerance ; by contrast, expression of the SOCS1 mutants had no effect
Ueki et al., Mol Cell Biol 2004 (Endotoxemia...) : Direct overexpression of SOCS-3 in liver by adenoviral mediated gene transfer markedly decreases tyrosine phosphorylation of both IRS-1 and IRS-2, while SOCS-1 overexpression preferentially inhibits IRS-2 phosphorylation
Jamieson et al., J Biol Chem 2005 (Hypoglycemia...) : Socs1 deficiency increases IRS-2 expression and enhances hepatic insulin sensitivity in vivo indicating that inhibition of SOCS1 may be a logical strategy in type 2 diabetes