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STAT3 — TGFB1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Ogata et al., Oncogene 2006
(Carcinoma, Hepatocellular...) :
Loss of SOCS3 in the liver promotes fibrosis by enhancing
STAT3 mediated
TGF-beta1 production
Kinjyo et al., J Exp Med 2006
(Leishmaniasis, Cutaneous) :
We found that
STAT3 positively
regulates TGF-beta1 promoter activity depending on the potential STAT3 binding sites
Yang et al., Cancer Res 2006
:
The results indicate that PKA is an upstream regulator for
TGF-beta1 induced
STAT3 activation and plays an important role in TGF-beta1 mediated apoptosis and EMT
Ruff et al., BMC cancer 2007
(Lymphoma, AIDS-Related...) :
IL-6 was shown to activate
STAT3 , even in the
presence of
TGF-beta1 , and thereby to activate proliferative and anti-apoptotic pathways ... Like LCL-8664, UMCL01-101 was sensitive to TGF-beta1 mediated inhibition, rescued partially by IL-6, and demonstrated rapid
STAT3 activation following IL-6 treatment even in the
presence of
TGF-beta1
Yu et al., Int J Biochem Cell Biol 2008
:
SOCS 3 and PPAR-gamma ligands
inhibit the expression of IL-6 and
TGF-beta1 by regulating
JAK2/STAT3 signaling in pancreas
Wasik et al., Semin Oncol 2009
(Cell Transformation, Neoplastic...) :
Recent data indicate that NPM/ALK also promotes immune evasion of the ALK ( + ) TCL by inducing through
STAT3 activation the expression of immunosuppressive cytokines interleukin-10 (IL-10) and
transforming growth factor-beta ( TGFss ) and cell surface protein CD274 ( PD-L1, B7-H1 )
Pan et al., Hepatology 2009
:
NO and FCCP also inhibited
TGF-beta1 induced
STAT3 activation, suggesting that signal transducer and activator of transcription 3 inactivation is involved in the NO-induced effects on TGF-beta1 induced EMT and apoptosis