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INSR — PI3
Text-mined interactions from Literome
Benzeroual et al., Biochim Biophys Acta 2000
:
Our data demonstrate that the
stimulation of
PI 3-kinase activity by the activated
insulin receptor , but not the phosphorylation of IR beta-subunit and IRS-1, requires an influx of Ca ( 2+ )
Goldfine et al., Metabolism 2000
(Diabetes Mellitus, Type 2) :
Vanadyl modifies proteins in human skeletal muscle involved in early insulin signaling, including basal
insulin receptor and substrate tyrosine phosphorylation and
activation of
PI 3-kinase , and is not additive or synergistic with insulin at these steps
Hers et al., Biochem J 2002
:
Furthermore, insulin induced insulin receptor tyrosine phosphorylation, phosphorylation of Tyr ( 1158 ) and
insulin receptor tyrosine kinase activity were all
reduced by inhibition of
PI 3-kinase at later time points ( > or=20 min )
Ogihara et al., Hypertension 2002
(Hyperinsulinism...) :
Despite the insulin resistance, insulin induced tyrosine phosphorylation of the insulin receptor and
insulin receptor substrates,
activation of
phosphatidylinositol (PI) 3-kinase , and phosphorylation of Akt were all enhanced by AII infusion
Kanda et al., Biochem Biophys Res Commun 2003
:
However, VEGFR-2,
insulin receptor substrate-1, and c-Src were also
involved in VEGF-A induced activation of
PI3-kinase , resulting in the compensation in cells expressing kinase-inactive c-Fes
Fisslthaler et al., Nitric Oxide 2003
:
Insulin applied to native porcine aortic endothelial cells elicited the tyrosine phosphorylation of the
insulin receptor and receptor substrate, the subsequent
activation of
phosphatidylinositol 3-kinase (PI 3-K) , Akt ( protein kinase B ), and ERK1/2
Rajala et al., Mol Neurobiol 2003
:
This article, describes recent studies that link the photobleaching of rhodopsin to tyrosine phosphorylation of the
insulin receptor and subsequent
activation of
phosphoinositide 3- kinase (PI3K)
Chang et al., J Biol Chem 1995
:
We conclude that ( i ) transgenic expression of kinase-defective insulin receptors exerts dominant negative effects at the level of receptor auto-phosphorylation and kinase activation ; ( ii )
insulin receptor tyrosine kinase activity is
required for in vivo insulin stimulated IRS-1 phosphorylation, IRS-1 associated
PI 3-kinase activation, phosphorylation of mitogen activated protein kinase, and c-fos gene induction in skeletal muscle ; ( iii ) hybrid receptor formation is likely to contribute to the in vivo dominant negative effects of kinase-defective receptor expression
Yenush et al., Mol Cell Biol 1996
:
IRS-1 was
required by the human
insulin receptor to activate
PI 3-kinase and p70s6k, whereas hDIR associated with PI 3-kinase and activated p70s6k without IRS-1