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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