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AKT1 — IARS

Text-mined interactions from Literome

Rui et al., J Biol Chem 2001 (Carcinoma, Hepatocellular...) : By contrast, IRS-1 activation of Akt and ERK1/2 was not inhibited by chronic insulin/IGF-1 stimulation in IRS-2-deficient mouse embryo fibroblasts
Kaburagi et al., Biochem Biophys Res Commun 2003 : Overexpressed IRS-3 as well as IRS-1 enhanced phosphoinositide (PI) 3-kinase activity in response to insulin and increased phosphorylation of protein kinase B (PKB) at S473 and phosphorylation of one of the members of the forkhead transcription factor FKHRL1 on T32 in both insulin untreated and -treated states
Stenkula et al., Mol Cell Endocrinol 2004 : We found that IRS-3F4 blocked insulin stimulation of HA-PKB/Akt phosphorylation and in further analyses also translocation of recombinant HA-tagged glucose transporter to the plasma membrane ... We found that IRS-3F4 blocked insulin stimulation of HA-PKB/Akt phosphorylation and in further analyses also translocation of recombinant HA-tagged glucose transporter to the plasma membrane
Steppan et al., Mol Cell Biol 2005 (Insulin Resistance) : Here we show that in 3T3-L1 adipocytes, resistin attenuates multiple effects of insulin, including insulin receptor (IR) phosphorylation, IR substrate 1 (IRS-1) phosphorylation, phosphatidylinositol-3-kinase (PI3K) activation, phosphatidylinositol triphosphate production, and activation of protein kinase B/Akt ... Here we show that in 3T3-L1 adipocytes, resistin attenuates multiple effects of insulin, including insulin receptor (IR) phosphorylation, IR substrate 1 (IRS-1) phosphorylation, phosphatidylinositol-3-kinase (PI3K) activation, phosphatidylinositol triphosphate production, and activation of protein kinase B/Akt
Kim et al., Endocrinology 2005 (Neuroblastoma) : In summary, 1 ) IRS-2 is more sensitive to IGF-I mediated degradation ; 2 ) IRS degradation is mediated by phosphatidylinositol 3-kinase and proteasome sensitive pathways ; and 3 ) high levels of IGF-IR, and possibly the subsequent increase in Akt phosphorylation, are required for efficient IRS degradation
Asano et al., Cancer Res 2005 (Pancreatic Neoplasms) : Furthermore, IRS-1 was phosphorylated on a p85 binding site ( Y ( 612 ) ), and IRS-specific small interfering RNA potently inhibited activation of PI3K and Akt in transfected cells
Luna et al., Diabetologia 2006 (Diabetes Mellitus, Type 2) : In contrast, IRS-1 dependent phosphatidylinositol (PI) 3-kinase activity and Ser473 phosphorylation of protein kinase B were not altered by metformin therapy, whereas the responsiveness of muscle aPKC to PI-3,4,5- ( PO ( 4 ) ) ( 3 ), the lipid product of PI 3-kinase, was improved
Muñoz et al., J Hypertens 2006 (Disease Models, Animal...) : We found that in the livers of OZR long-term administration of irbesartan is associated with : ( i ) increased insulin stimulated insulin receptor tyrosine phosphorylation ; ( ii ) decreased insulin receptor Ser994 phosphorylation ; ( iii ) augmented insulin receptor substrate (IRS) 1 and 2 abundance and tyrosine phosphorylation ; ( iv ) augmented association between IRS and the p85 regulatory subunit of phosphatidylinositol 3-kinase ; ( v ) increased insulin induced Akt phosphorylation ; and ( vi ) decreased hepatic steatosis
Biswas et al., Molecular vision 2009 : Together, these data indicate that disruption of PDGF receptor signaling compromises the pro-survival effect of insulin induced IRS dependent PI 3-kinase/Akt signaling in RGCs, and that the maintenance of PDGF induced PI 3-kinase/Akt signaling is critical for the survival of retinal neuronal cells
Tsunekawa et al., Diabetes 2011 : Activation of IRS signaling in isolated rat islets by insulin/IGF-I ( used as an experimental in vitro tool ) or downstream constitutive activation of protein kinase B (PKB) significantly decreased IRS-2 expression