IndraLab
Statements
sparser
"This action involved a PR (proline rich) domain-dependent interaction of PRR11 with the p85 regulatory subunit of PI3K which reduces homodimerization of p85 and, in turn, is permissive of ligand-induced association of p110α with insulin receptor substrate 1 (IRS1) and activation of PI3K. Ectopic expression of PRR11 failed to promote estrogen-independent growth when p110α was knocked down, and PRR11 -overexpressing cells were highly sensitive to PI3K inhibitors, suggesting that PRR11 amplification generates dependence on PI3K signaling, particularly in the setting of estrogen deprivation."
reach
"In support of earlier results, it was also notable that the stapled mutant peptide did slightly reduce the protein levels of p110alpha, but did not affect levels of p85 and IRS1 (XREF_FIG and XREF_SUPPLEMENTARY), providing further evidence that the protein interaction between mutant p110alpha and IRS1 stabilizes p110alpha."
IRS1 binds PIK3CA and kinase domain. 2 / 2
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"As expected, compared with normal chow-fed mice, insulin-induced AKT phosphorylation, tyrosine phosphorylation of IRS1 (insulin receptor substrate 1), and IRS1 interaction with p85-phosphoinositide 3 kinase (PI3K) were greatly reduced in adipose tissue, liver, and muscle of HFD-fed wild-type control mice ( xref ), demonstrating diet-induced insulin insensitivity of these tissues."