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IKBKB — TLR2
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Wang et al., Infect Immun 2001
:
These data indicate that micrococci and PGN induce
TLR2 dependent activation of the gene for IL-8 and that this activation
requires MyD88, IRAK, NIK,
IKK , and NF-kappaB and may also utilize TRAF6 and, to a lesser extent, TRAF2
Chen et al., Biochem Biophys Res Commun 2004
:
Nontypeable Haemophilus influenzae lipoprotein P6 induces MUC5AC mucin transcription via
TLR2-TAK1 dependent p38 MAPK-AP1 and
IKKbeta-IkappaBalpha-NF-kappaB signaling pathways ... Moreover, P6 induces MUC5AC transcription via
TLR2-MyD88-IRAK1-TRAF6-TAK1 dependent p38 MAPK-AP1 and
IKKbeta-IkappaBalpha-NF-kappaB signaling pathways
Caricilli et al., J Endocrinol 2008
(Insulin Resistance) :
In addition, data show that the inhibition of
TLR2 expression
prevents the activation of
IKBKB , MAPK8, and serine phosphorylation of IRS1 in DIO mice, suggesting that TLR2 is a key modulator of the crosstalk between inflammatory and metabolic pathways
Chiu et al., Chem Biol Interact 2009
:
Propofol inhibits lipoteichoic acid induced iNOS gene expression in macrophages possibly through downregulation of
toll-like receptor 2-mediated activation of
Raf-MEK1/2-ERK1/2-IKK-NFkappaB
Tong et al., Cell Res 2012
:
NLRC5 ablation reduces MHC class I expression, and enhances
IKK and IRF3 phosphorylation in
response to
TLR stimulation or viral infection