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IARS — IGF1
Text-mined interactions from Literome
Tsuruzoe et al., Mol Cell Biol 2001
(MAP Kinase Signaling System) :
In these cell lines,
IGF-1 caused the rapid tyrosine phosphorylation of all four
IRS proteins
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
Lingohr et al., Mol Cell Endocrinol 2003
:
In contrast,
glucose/IGF-1 induced Erk-1/-2 and p70S6K activation were unaffected by
IRS-3
Hoang et al., Cancer Res 2004
(MAP Kinase Signaling System...) :
IGF-I stimulation of cells
resulted in enhanced activation of type I IGF receptor and
IRS adaptor proteins
Laurino et al., J Cell Sci 2005
:
Our results show that
IGF-1 , but not BDNF, significantly and rapidly
stimulates IRS/PI3K/Akt and membrane expansion
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
Simmons et al., Am J Physiol Gastrointest Liver Physiol 2007
:
In intestinal epithelial cells,
IRS-1 was expressed at higher levels than IRS-2 and was preferentially
activated by
IGF-I
Becker et al., Mol Endocrinol 2011
(Breast Neoplasms) :
Although rapamycin induced mTOR inhibition has been shown to block
IGF induced
IRS degradation, we reveal differential effects on motility ( up-regulation ) and proliferation ( down-regulation )
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
Takata et al., Metabolism 1996
:
IGF-I normally
stimulated receptor autophosphorylation,
IRS-I phosphorylation, and glycogen synthesis in cells expressing Asp 1048 IR