◀ Back to LEP
LEP — STAT1
Text-mined interactions from Literome
Wolf et al., Kidney Int 1999
(Glomerulosclerosis, Focal Segmental) :
Leptin also
stimulated phosphorylation of
STAT1alpha , and kinase inhibitors attenuated proliferation, suggesting a pivotal role of phosphorylation in this process
Bendinelli et al., Mol Cell Endocrinol 2000
:
Leptin activates Stat3,
Stat1 and AP-1 in mouse adipose tissue
Scarpace et al., Neuroscience 2001
(Disease Models, Animal...) :
There were no changes in total STAT3 protein with leptin or age, and
leptin did not
increase phosphorylation of
STAT1
Maccarrone et al., J Biol Chem 2003
:
Leptin binding to the receptor
triggered activation of STAT3 but not
STAT1 or STAT5 or the mitogen activated protein kinases p38, p42, and p44
Pan et al., J Mol Neurosci 2007
(Obesity) :
Leptin signaling by ObRb
caused a large increase of both
Stat1 and Stat3, and this was significantly potentiated by the addition of urocortin, being more robust for Stat3 than Stat1
Kanda et al., Endocrinology 2008
:
IL-1beta enhanced the transcriptional activity of NF-kappaB, whereas
leptin enhanced
STAT1 and STAT3 activity ... The p38 MAPK inhibitor SB202190 suppressed IL-1beta- and IL-1beta plus leptin induced hBD-2 production, IL-1beta induced NF-kappaB activity, and
leptin induced
STAT1 and STAT3 activity ; contrastingly, the Janus kinase (JAK) 2 inhibitor AG490 suppressed IL-1beta plus leptin induced hBD-2 production and leptin induced STAT1 and STAT3 activity
McCowen et al., Endocrinology 1998
:
By contrast,
leptin did not
increase the phosphorylation of Janus kinase proteins, mitogen activated protein kinase, or
STAT1 and -5 despite abundant expression of these signaling molecules in the hypothalamus