◀ Back to INSR
INSR — SOCS3
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
Complex of INSR-STAT5B
→
SOCS3
(decreases)
Emanuelli et al., J Biol Chem 2000*
Evidence: this negative regulation likely results from competition between SOCS3 and Stat5B binding to the same insulin receptor motif SOCS3 binds to the insulin receptor at phosphotyrosine 960, which is precisely where Stat5B binds
-
OpenBEL Selventa BEL large corpus:
Complex of INSR-STAT5B
→
SOCS3
(decreases)
Evidence: SOCS-3 binds to JAK proteins with very low affinity although SOCS-3 has no effect on insulin receptor tyrosine kinase activity, it binds to the insulin receptor at Y960 and prevents STAT5B binding
-
OpenBEL Selventa BEL large corpus:
Complex of INSR-SOCS3
→
STAT5B
(decreases)
Emanuelli et al., J Biol Chem 2000*
Evidence: this negative regulation likely results from competition between SOCS3 and Stat5B binding to the same insulin receptor motif SOCS3 binds to the insulin receptor at phosphotyrosine 960, which is precisely where Stat5B binds
-
KEGG Insulin signaling pathway:
SOCS1/SOCS2/SOCS3/SOCS4
→
INSR
(protein-protein, inhibition)
-
KEGG Type II diabetes mellitus:
SOCS1/SOCS2/SOCS3/SOCS4
→
INSR
(protein-protein, inhibition)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
SOCS3
—
INSR
(physical association, affinity chromatography technology)
Calegari et al., Endocrinology 2005*
-
IRef Biogrid Interaction:
SOCS3
—
INSR
(physical association, affinity chromatography technology)
Senn et al., J Biol Chem 2003*
-
IRef Hprd Interaction:
SOCS3
—
INSR
(two hybrid)
Dey et al., Biochem Biophys Res Commun 2000*, Senn et al., J Biol Chem 2003*
-
IRef Hprd Interaction:
SOCS3
—
INSR
(in vitro)
Dey et al., Biochem Biophys Res Commun 2000*, Senn et al., J Biol Chem 2003*
-
IRef Ophid Interaction:
SOCS3
—
INSR
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
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
Ghanim et al., Diabetologia 2007
(Inflammation...) :
The increase in
SOCS3 but not IKBKB or PRKCB2 is related inversely to p-INSR-beta and might
mediate the inhibition of
p-INSR-beta