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POMC — STAT3
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Bousquet et al., J Clin Invest 2000
:
Direct
regulation of pituitary
proopiomelanocortin by
STAT3 provides a novel mechanism for immuno-neuroendocrine interfacing ... Whereas pathways shown thus far to regulate POMC expression exclusively involve cAMP or calcium, we here describe a direct and indirect
STAT3 dependent regulation of
POMC transcription by LIF ... We therefore conclude that both a direct and indirect route mediate LIF induced
STAT3 activation of
POMC transcription ... Demonstration of
STAT3 dependent regulation of the
POMC gene represents a powerful mechanism for immuno-neuroendocrine interfacing and implies a direct stimulation of ACTH secretion by inflammatory and stress derived STAT3 inducing cytokines
Auernhammer et al., Endocrinology 2003
:
In comparison with mock transfected cells, stable overexpression of SOCS-3 in AtT-20 cells abolished NNT-1/BSF-3 induced STAT1 and
STAT3 phosphorylation and almost completely
inhibited STAT dependent
proopiomelanocortin promoter and SOCS-3 promoter activities
Mori et al., Nat Med 2004
(Insulin Resistance...) :
Compared to their wild-type littermates, Socs3-deficient mice showed enhanced leptin induced hypothalamic
Stat3 tyrosine phosphorylation as well as
pro-opiomelanocortin (POMC) induction , and this resulted in a greater body weight loss and suppression of food intake
Xu et al., Endocrinology 2007
(Obesity...) :
We find that Pomc expression is diminished in the mutant mice, suggesting that
Stat3 is
required for
Pomc transcription ... These results demonstrate a
requirement for
Stat3 in transcriptional regulation of
Pomc but indicate that this circuit is only one of several components that underlie the neuronal response to leptin and the role of Stat3 in that response
Fan et al., Endocrinology 2008
(Body Weight) :
In vitro, AR significantly enhanced
STAT3 mediated transcription of leptin target genes including
POMC and SOCS3
Yang et al., J Biol Chem 2009
:
FoxO1
inhibits leptin regulation of
pro-opiomelanocortin promoter activity by blocking
STAT3 interaction with specificity protein 1 ... We show that
phospho-STAT3 activates
POMC promoter in response to leptin signaling through a mechanism that requires an SP1 binding site in the POMC promoter
Ernst et al., J Neurosci 2009
(Body Weight...) :
While
Stat3 activation in POMC neurons is
required for
POMC expression, the role of elevated basal Stat3 activation as present in the development of obesity has not been directly addressed ... These data indicate that constitutive
Stat3 activation is not
sufficient to promote
POMC expression but requires simultaneous PI3K ( phosphoinositide 3-kinase ) -dependent release of FOXO1 repression
Shi et al., Diabetologia 2013
(Inflammation) :
Finally, RELA binds to STAT3 and inhibits STAT3 mediated promoter activity, suggesting that RELA, possibly together with forkhead box containing protein 1 ( FOXO1 ), may prevent
STAT3 mediated leptin
activation of the
Pomc promoter