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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