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FOS — TLR4
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Fan et al., Shock 2004
(Inflammation...) :
Pretreatment with PTx inhibited
TLR4ca induced ERK 1/2 phosphorylation ( 30 +/- 7 %, P < 0.05 ) and
AP-1 activation ( 36 +/- 3 %, P < 0.05 ) but did not inhibit NFkappaB activation
Roger et al., Biochem J 2005
:
Critical
role for Ets,
AP-1 and GATA-like transcription factors in regulating mouse
Toll-like receptor 4 (Tlr4) gene expression
Wang et al., Nat Immunol 2006
:
Tumor necrosis factor receptor associated factor 6 ( TRAF6 ) is critical for mediating
Toll-like receptor ( TLR ) -interleukin 1 receptor (IL-1R) signaling and subsequent
activation of NF-kappaB and
AP-1 , transcriptional activators of innate immunity
Wolf et al., J Am Soc Nephrol 2006
(Inflammation) :
Reporter gene experiments indicate that an
activating protein-1 (AP-1) as well as an E-26 specific sequence ( Ets ) binding site in the TLR4 promoter are
responsible for the AngII stimulated transcriptional activity of the
TLR4 gene
Oak et al., J Immunol 2006
(Inflammation...) :
In contrast, JNK phosphorylation as well as
AP-1 nuclear binding were augmented by acute alcohol in the
presence of combined
TLR4 and TLR2 stimulation
Hu et al., J Leukoc Biol 2007
:
IFN-gamma suppression of
TLR induced activation of
AP-1 and downstream target genes challenges current concepts about the inflammatory role of AP-1 proteins in macrophage activation and is consistent with a role for AP-1 in the generation of noninflammatory osteoclasts
Wen et al., J Exp Med 2010
(Peritonitis...) :
Rac1 activation is accompanied by JNK ( c-Jun N-terminal kinase ) and NF-?B activation, culminating in
TLR induced binding of NF-?B and
AP-1 to the promoters of inflammatory cytokines
Meldrum et al., J Biol Chem 2012
(Fibrosis...) :
TLR4 promotor activity, as well as
AP-1 activation and the
effect of AP-1 knockdown on
TLR4 expression, was evaluated in HK-2 cells in response to IL-18 stimulation
Yang et al., Lab Invest 2013
(Acute Lung Injury...) :
Inhibition of
TLR4 expression in the lung tissue by infection with pGCSIL-GFP-lentivirus expressing small hairpin RNAs targeting the TLR4 gene ( TLR4-shRNA lentivirus ) significantly
attenuated ALI, lung inflammation, and activity of p38MAPK and
AP-1 in the lung tissue