◀ Back to STAT3
INS — STAT3
Text-mined interactions from Literome
Carvalheira et al., Biol Chem 2003
:
Acutely injected
insulin stimulated a mild increase in tyrosine phosphorylation of JAK2,
STAT3 and STAT5b
Kuwahara et al., Mol Cell Endocrinol 2003
(Carcinoma, Hepatocellular...) :
Insulin inhibits leptin induced
STAT3 phosphorylation in a time- and dose dependent manner without affecting Janus tyrosine kinases ( JAKs ) JAK2 phosphorylation
Fujita et al., Experimental biology and medicine (Maywood, N.J.) 2003
(Anorexia...) :
Insulin and glucose icv
resulted in reduction of leptin induced
STAT3 tyrosine phosphorylation compared with saline
Gorogawa et al., Biochem Biophys Res Commun 2004
(Body Weight...) :
Our present observations demonstrate a unique
role of
STAT3 in maintaining glucose mediated early-phase
insulin secretion and normal islet morphology
Benomar et al., Biochem J 2005
:
Insulin or leptin pre-treatment of SH-SY5Y cells
increased basal
STAT-3 phosphorylation, but abolished the acute effect of these hormones, and, interestingly, leptin pre-treatment abolished insulin effect and vice versa
Benomar et al., Mol Cell Endocrinol 2005
(Body Weight...) :
Leptin infusion also abolished
STAT-3 phosphorylation in
response to
insulin or leptin and similar results were obtained for MAP-kinase phosphorylation
Zhang et al., Mol Cell Biol 2006
:
Insulin induces multiprotein complex formation of RACK1, IR, and
STAT3 ... Site-specific mutants of IR and IGF-1R impaired in RACK1 binding are ineffective in mediating recruitment and
activation of
STAT3 as well as in
insulin- or IGF-1 induced protection of cells from anoikis
Gartsbein et al., J Cell Sci 2006
:
Activated forms of PKCdelta and STAT3 were essential for
insulin induced
PKCdelta-STAT3 activation in keratinocyte proliferation ... Abrogation of PKCdelta activity inhibited
insulin induced
STAT3 phosphorylation, PKCdelta-STAT3 association and nuclear translocation ... Finally, overexpression of a STAT3 serine mutant abrogated
insulin induced
STAT3 serine phosphorylation and STAT3 induced keratinocyte proliferation, whereas STAT3 tyrosine phosphorylation was induced and nuclear localization remained intact
Inoue et al., Cell Metab 2006
(Insulin Resistance) :
This effect of insulin was mediated by the hormone 's effects in the brain, and the increase in hepatic IL-6 induced by the
brain-insulin action is
essential for the activation of
STAT3
Andersson et al., J Biol Chem 2007
:
Insulin reduces the tyrosine phosphorylation and
increases the serine phosphorylation of
STAT3 , thereby reducing its nuclear localization and transcriptional activity
Roberts et al., J Cell Biochem 2007
:
PD98059 enhanced
insulin , cytokine, and growth factor activation of xanthine oxidoreductase in epithelial cells
involves STAT3 and the glucocorticoid receptor
Boonsong et al., Biochem Soc Trans 2007
:
Neither exercise nor
insulin affected
STAT3 ( signal transducer and activator of transcription 3 ) or p38 MAPK ( mitogen activated protein kinase ) phosphorylation
Kim et al., J Biol Chem 2008
(Carcinoma, Hepatocellular...) :
Interestingly, we find that the phosphorylation of STAT3 on Ser ( 727 ) and STAT3 transcriptional activity are regulated by mTOR upon IL-6 stimulation and that
STAT3 is
required for IL-6 inhibition of
insulin signaling
Fuglesteg et al., Basic Res Cardiol 2008
(Disease Models, Animal...) :
Insulin given at reperfusion
led to phosphorylation of
STAT3 and Akt both of which were inhibited by AG490
Won et al., Obesity (Silver Spring) 2009
(Obesity) :
ICV administration of TG by itself activated signal-transduction-activated-transcript-3 ( STAT3 ) and Akt in the hypothalamus, but prevented a further
activation of hypothalamic
STAT3 and Akt by leptin and
insulin
Kim et al., J Biol Chem 2009
(Diabetes Mellitus, Type 2...) :
Replacement of the endogenous STAT3 with wild-type, but not S727A, recombinant
STAT3 restored the ability of amino acids to inhibit
insulin signaling, suggesting that Ser ( 727 ) phosphorylation was critical for STAT3 mediated amino acid effect ... Furthermore, overexpression of
STAT3-S727D was
sufficient to inhibit
insulin signaling in the absence of excess amino acids
Ceresa et al., J Biol Chem 1996
:
Immuno-precipitation of STAT1 and STAT3 from 32P labeled cells demonstrated that only
STAT3 was phosphorylated in
response to
insulin whereas phosphoamino acid analysis indicated that this phosphorylation event occurred exclusively on serine residues ... Together, these data demonstrate that
insulin is a specific
activator of
STAT3 serine phosphorylation without affecting the other STAT isoforms
Ceresa et al., Endocrinology 1997
:
We recently reported that
insulin stimulation
results in the serine phosphorylation of
STAT3 ( signal transducer and activator of transcription-3 ) ... In the present study, we identified serine 727 as the site of
insulin stimulated
STAT3 serine phosphorylation ... Blockade of ERK activation by expression of the MAP kinase phosphatase ( MKP-1 ) had no effect on
insulin stimulated
STAT3 serine phosphorylation ... Together, these data demonstrate that the
insulin stimulated serine phosphorylation of
STAT3 occurs by a MEK dependent pathway that is independent of ERK activation
Coffer et al., Oncogene 1997
:
Insulin activates
Stat3 independently of p21ras-ERK and PI-3K signal transduction ... Utilising a dominant negative mutant of p21ras we demonstrate that both
insulin induced
Stat3 DNA binding and also transactivation do not require p21ras ... Furthermore, although previous studies have suggested a role for MAP kinases ( ERKs ) and PI-3K in STAT activation, utilising the specific MEK inhibitor PD098059 and the PI-3K inhibitor wortmannin, we demonstrate that activation of ERKs or PI-3K are not required for
insulin induced
Stat3 phosphorylation or transactivation