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JUN — TLR9
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)
Hong et al., Int Immunopharmacol 2004
(Disease Models, Animal...) :
Furthermore, CQ reduced the expression of
TLR9 and TLR4 mRNA and the
activation of NFkappaB and
AP-1 stimulated by CpG ODN and LPS in ANA-1 cells
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
Guo et al., J Immunol 2005
:
This study illustrates the crucial
roles for
AP-1 , IRF-1, IRF-2, and STAT1 in the regulation of murine
TLR9 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
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
El Kebir et al., Arch Immunol Ther Exp (Warsz) 2008
(Bacterial Infections) :
TLR9 stimulation
results in alterations in cellular redox balance, peroxynitrite formation, activation of the mitogen activated protein kinase, PI3-kinase, and Jun N-terminal kinase pathways and/or nuclear factor kappaB and
AP-1
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