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IRS1 — POLDIP2
Text-mined interactions from Literome
Garrouste et al., Cell Death Differ 2002
:
In this model, IGF-I did not activate the focal adhesion kinase, whereas it induced tyrosine phosphorylation of the
insulin receptor substrate-1 and
activation of the extracellular signal related kinase 1 and 2,
p38 , phosphatidylinositol 3'-kinase and protein kinase B/Akt
Hers et al., Biochem J 2005
:
Furthermore, inhibition of mTOR/p70S6 kinase, JNK or
p38MAPK had no effect on insulin stimulated
IRS-1 tyrosine phosphorylation
Carlson et al., Metabolism 2005
(Insulin Resistance) :
However,
p38 inhibition did not
prevent the loss of
IRS-1 protein levels or insulin signaling to PKB in insulin-resistant cells
Hemi et al., Diabetes 2011
(Insulin Resistance) :
Liver expression of dominant negative ( DN )
-p38MAPKa in ob/ob mice
reduced fasting insulin levels and improved glucose tolerance, whereas C57/BL6 mice overexpressing wild-type p38MAPKa exhibited enhanced IRS-1 serine phosphorylation and reduced insulin stimulated
IRS-1 tyrosine phosphorylation