◀ Back to TCF23
TCF23 — TLR2
Text-mined interactions from Literome
Medvedev et al., J Immunol 2000
(MAP Kinase Signaling System) :
In this study, the effect of in vitro endotoxin tolerance on LPS induced mitogen activated protein kinase activation,
transcription factor induction , and cytokine, chemokine, and
Toll-like receptor (TLR) 2 and 4 gene expression, as well as the involvement of TNF and IL-1 signaling pathways in tolerance, were examined
Tachado et al., J Leukoc Biol 2007
:
In human AM, Pc promoted direct interaction of MR and
TLR2 , IL-8 release was reduced markedly upon simultaneous blocking of TLR2 and gene silencing of MR, and IL-8 release was
dependent in part on
transcription factor NF-kappaB and ERK1/2 and JNK MAPKs
Goodridge et al., Handb Exp Pharmacol 2008
:
This review focuses on the
role ( s ) of
TLR2 and Dectin-1 in triggering inflammatory responses,
transcription factor activation, phagocytosis, and reactive oxygen production in response to fungi
Scanzello et al., Curr Opin Rheumatol 2008
(Chronic Disease...) :
TLRs are expressed and functional in the joint, and many proteases and cytokines that promote cartilage catabolism are dependent on nuclear factor-kappaB, a
TLR activated
transcription factor
Sun et al., Circ Res 2009
:
TLR signaling via p38
led to phosphorylation and activation of the
transcription factor Microphthalmia transcription factor, acting at E-box elements in the Ctsk promoter
Li et al., Int Immunopharmacol 2010
(Inflammation...) :
In conclusion, our results demonstrated that AS-mediated protection on septic mice challenged with S. aureus was associated with its reduction on TNF-alpha release via inhibition of
TLR2 and Nod2 mRNA expressions and
transcription factor NF-kappaB
activation
Mohammad et al., Exp Eye Res 2013
(Diabetes Mellitus, Experimental...) :
Diabetes
induced significant upregulation of the expression of HMGB-1, receptor for advanced glycation end products ( RAGE ), ERK ( 1/2 ) and nuclear
transcription factor Kappa B ( NF-?B ), whereas the expression of
toll-like receptor 2 (TLR2) and occludin was significantly downregulated