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IRS1 — SOCS3
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Ridderstråle et al., Horm Metab Res 2003
:
With overexpression of GHR, Jak2 and IRS-1 along with each of these SOCS proteins in human A293 cells, we could demonstrate that both SOCS-1 and
SOCS-3 completely
inhibited the GH-stimulated tyrosine phosphorylation of
IRS-1 , whereas SOCS-2 and CIS did not
Shi et al., J Biol Chem 2004
:
By using SOCS3-deficient adipocytes differentiated from mouse embryonic fibroblasts, we found that
SOCS3 deficiency
increases insulin stimulated
IRS1 and IRS2 phosphorylation, IRS associated phosphatidylinositol 3-kinase activity, and insulin stimulated glucose uptake
Calegari et al., Endocrinology 2005
:
The inhibition of
SOCS-3 expression by a phosphorthioate modified antisense oligonucleotide partially
restores angiotensin II-induced inhibition of insulin induced insulin receptor,
IRS-1 and IRS-2 tyrosine phosphorylation, and IRS-1 and IRS-2 association with p85-phosphatidylinositol 3-kinase and [ Ser473 ] phosphorylation of Akt
Shi et al., Diabetes 2006
(Insulin Resistance) :
In adipocytes, suppressor of cytokine signaling
(SOCS)3 deficiency
increases insulin stimulated insulin receptor substrate
(IRS)-1 and -2 phosphorylation, IRS associated phosphatidylinositol 3 kinase activity, and insulin stimulated glucose uptake ... Moreover,
SOCS3 is
required for tumor necrosis factor-alpha full inhibition of insulin stimulated
IRS-1 and -2 phosphorylation, phosphatidylinositol 3 kinase activity, and glucose uptake
Ishizuka et al., Endocrinology 2007
(Insulin Resistance) :
Serine phosphorylation of insulin receptor substrate
(IRS)-1 and the
induction of
suppressor of cytokine signaling 3 ( SOCS3 ) is recently well documented as the mechanisms for the insulin resistance ... However, low-level expression of
SOCS3 by IL-6 or adenovirus vector did not
affect insulin stimulated
IRS-1 tyrosine phosphorylation ... Interestingly, when
IRS-1 serine phosphorylation was enhanced by TNFalpha or anisomycin in the
presence of low-level
SOCS3 , IRS-1 degradation was remarkably enhanced ... Taken together, both
IRS-1 serine phosphorylation and
SOCS3 induction are necessary, but one of the pair is not sufficient for the inhibited insulin signaling ... Chronic TNFalpha may inhibit insulin signaling effectively because it causes both
IRS-1 serine phosphorylation and the following
SOCS3 induction in 3T3-L1 adipocytes
Ko et al., Diabetes 2009
(Diabetic Angiopathies...) :
Acute physiological elevation of IL-6 suppressed glucose metabolism and caused insulin resistance by increasing SOCS3 and via
SOCS3 mediated inhibition of insulin receptor substrate
(IRS)-1 and possibly AMPK in heart
Yang et al., Mol Cell Biochem 2010
:
The results showed that 100 nM insulin could induce SOCS3 mRNA expression but not protein expression, and overexpression of
SOCS3 decreased IRS1 protein level, insulin stimulated IRS1 tyrosine phosphorylation, PI3K activation, and Akt phosphorylation, but
increased IRS1 serine phosphorylation in porcine primary adipocytes
Li et al., PloS one 2013
:
These data suggest that serine phosphorylation of
IRS-1 in response to inflammation is
mediated , in part, by NF-?B, JNK and
SOCS3