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IRS1 — SOCS1
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 *
-
IRef Biogrid Interaction:
SOCS1
—
IRS1
(physical association, affinity chromatography technology)
Li et al., Cell Signal 2007*
-
IRef Biogrid Interaction:
SOCS1
—
IRS1
(physical association, affinity chromatography technology)
Rui et al., J Biol Chem 2002*
-
IRef Hprd Interaction:
SOCS1
—
IRS1
(in vitro)
Kawazoe et al., J Exp Med 2001*, Rui et al., J Biol Chem 2002*
-
IRef Hprd Interaction:
SOCS1
—
IRS1
(in vivo)
Kawazoe et al., J Exp Med 2001*, Rui et al., J Biol Chem 2002*
-
IRef Ophid Interaction:
SOCS1
—
IRS1
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Kawazoe et al., J Exp Med 2001
(Hypoglycemia) :
While the forced expression of
SSI-1 reduced the phosphorylation level of
insulin receptor substrate 1 (IRS-1) , SSI-1 deficiency resulted in sustained phosphorylation of IRS-1 in response to insulin.Furthermore, SSI-1 achieves this inhibition both by binding directly to IRS-1 and by suppressing Janus kinases ... These findings suggest that
SSI-1 acts as a negative feedback factor also in the insulin signal transduction pathway through the suppression of
IRS-1 phosphorylation
Rui et al., J Biol Chem 2002
(Insulin Resistance) :
Adenoviral mediated expression of
SOCS1 in mouse liver dramatically
reduced hepatic
IRS1 and IRS2 protein levels and caused glucose intolerance ; by contrast, expression of the SOCS1 mutants had no effect
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