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IRS2 — PTEN

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: IRS2 → PTEN (increases, IRS2 Activity) Simpson et al., Mol Cell Biol 2001*
  Evidence: PTEN induces cell cycle arrest and/or apoptosis associated with the downregulation of Akt activity and that dominant active Akt can rescue cells from PTEN inhibition In addition to showing increased levels, IRS-2 was tyrosine phosphorylated and associated with p85, proving that PTEN was able to stimulate the liganddependent activation of IRS-2 necessary for insulin signaling

Text-mined interactions from Literome

Simpson et al., Mol Cell Biol 2001 (Breast Neoplasms) : PTEN expression causes feedback upregulation of insulin receptor substrate 2 ... In addition, PTEN , LY294002, and rapamycin, an inhibitor of mammalian target of rapamycin, caused a reduction in the molecular weight of IRS-2 and an increase in the association of IRS-2 with PI3K ... Apparently, PTEN inhibits a negative regulator of IRS-2 to upregulate the IRS-2-PI3K interaction
Qin et al., Horm Metab Res 2009 (Disease Models, Animal...) : Quantitative real-time PCR assays showed that CE treatment decreased the mRNA expression of IL-1beta, IL-6 and TNF-alpha, improved the mRNA expression of IR, IRS1, IRS2 , PI3K and Akt1, inhibited CD36, MTTP, and PTEN , and enhanced the impaired SREBP-1c expression in TNF-alpha treated enterocytes