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LEPR — STAT3
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
Papathanassoglou et al., J Immunol 2006
:
Leptin binding to
ObR results in increased
STAT-3 activation in T cells, with a different activation pattern in resting vs anti-CD3 Ab stimulated T cells
Nair et al., Am J Respir Cell Mol Biol 2008
:
Leptin receptor expression and
activation of
STAT-3 , Src kinase, Suppressor of Cytokine Signaling-3 ( SOCS-3 ), and COX were evaluated by Western blotting and PCR
Gove et al., J Leukoc Biol 2009
(Colitis...) :
Role of
leptin receptor induced
STAT3 signaling in modulation of intestinal and hepatic inflammation in mice
Mancuso et al., J Immunol 2012
(Klebsiella Infections...) :
We recently reported that disruption of
leptin receptor mediated
STAT3 activation augmented host defense against pneumococcal pneumonia
Wu et al., J Cell Biochem 2013
(Liver Cirrhosis) :
Our results provide a new finding that HCVcp induced
ObR dependent Janus Kinase (JAK)
2-STAT3 , AMPKa, and AKT signaling pathways and modulated downstream fibrogenetic gene expression in HSCs. J. Cell
Leifheit-Nestler et al., Journal of translational medicine 2013
:
Our findings suggest that hearts from obese mice continue to respond to elevated circulating or cardiac leptin, which may mediate cardioprotection via
LepR induced
STAT3 activation, whereas signals distinct from LepR-Tyr1138 promote cardiac hypertrophy
Nakashima et al., FEBS Lett 1997
:
Stimulation of either a long form of
OB-R or gp130
led to tyrosine phosphorylation of
STAT3 , whereas stimulation of the truncated form of OB-R that is predominantly expressed in dbldb mice failed to do so