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IRS1 — PTEN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Nakashima et al., J Biol Chem 2000
(MAP Kinase Signaling System) :
Further, insulin induced phosphorylation of downstream targets Akt and p70S6 kinase were also inhibited significantly by overexpression of
PTEN , whereas tyrosine phosphorylation of the insulin receptor and
IRS-1 or the phosphorylation of mitogen activated protein kinase were not
affected , suggesting that the Ras/mitogen activated protein kinase pathway remains fully functional
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
Qin et al., Mol Nutr Food Res 2010
(Body Weight...) :
In the myocardium, GTP also increased the insulin receptor (Ir),
insulin receptor substrate 1 and 2 ( Irs1 and Irs2 ), phosphoinositide-3-kinase (Pi3k), v-akt murine thymoma viral oncogene homolog 1 ( Akt1 ), glucose transporter 1 and 4 ( Glut1 and Glut4 ) and glycogen synthase 1 (Gys1) expression but
inhibited phosphatase and tensin homolog deleted on chromosome ten ( Pten ) expression and decreased glycogen synthase kinase 3beta ( Gsk3beta ) mRNA expression
Clément et al., Hepatology 2011
(Carcinoma, Hepatocellular...) :
PTEN down-regulation
promoted in turn a reduction of
insulin receptor substrate 1 (IRS1) expression