◀ Back to TLR2
JUN — TLR2
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Janssens et al., FEBS Lett 2003
:
MyD88 is an adapter protein that is involved in
Toll-like receptor ( TLR ) - and interleukin-1 receptor (IL-1R) induced
activation of nuclear factor-kappaB (NF-kappaB) and
c-Jun N-terminal kinase (JNK)
Maloney et al., J Biol Chem 2005
(MAP Kinase Signaling System) :
Here, we show that A52R does not inhibit
TLR induced p38 or
c-Jun amino N-terminal kinase (JNK) mitogen activating protein ( MAP ) kinase activation
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
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
Chuang et al., Toxicol Lett 2009
:
Taken together, this study has shown that LPS selectively induces SP-A gene expression possibly through
TLR2 mediated activation of
c-Jun in human alveolar epithelial A549 cells
Zhu et al., Biochem J 2010
:
The mechanism was related to apoE suppression of
TLR-agonist induced phosphorylation of JNK ( c-Jun N-terminal kinase ) and
c-Jun
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
Hu et al., Cell Immunol 2013
:
Activation of
TLR2 inhibits chronic stress reduced phosphorylation of
c-Jun N-terminal kinase (JNK) and diminishes chronic stress induced up-regulation of corticosterone production