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PTGS2 — TLR3

Text-mined interactions from Literome

Pindado et al., J Immunol 2007 : Finally, cellular depletion of TLR3 by siRNA inhibits COX-2 expression, PGE2 generation, and iNOS induction by poly-IC
Lin et al., Mol Immunol 2010 : Nevertheless TLR mediated JNK activation as well as the increased protein expression of iNOS and COX-2 remained unchanged when Syk protein was knockdown by siRNA approach
Bernard et al., J Immunol 2010 : We hypothesized that Cox-2 is induced by TLR activation and is necessary for optimal AMP production, and that inhibitors of Cox-2 may therefore inhibit antimicrobial action
López et al., Int J Cardiol 2012 (Aortic Valve Stenosis...) : Strikingly, when TLRs sensing viral patterns were studied, a sustained TLR3 mediated activation of NF-?B, a ?B-independent induction of catalytically active cyclooxigenase (COX)-2 and ICAM-1 expression, and induction of expression of several chemokines were observed
Joseph et al., Biol Reprod 2013 (Inflammation) : Previously we reported the expression of prostaglandin-endoperoxide synthase 2 ( PTGS2 ), also known as cyclooxygenase 2 (COX-2), in human vaginal cells in response to toll-like receptor ( TLR ) ligands and other proinflammatory stimuli
Wu et al., PloS one 2013 : We showed that the hADSCs expressed Toll-like Receptors (TLR) 1, TLR2, TLR3 , TLR4, and TLR6 and that lipopolysaccharide (LPS) significantly induced the production of pro-inflammatory cytokines ( Cyclooxygenase-2 (Cox-2) , Interleukin-1ß (IL-1ß), Interleukin-6 (IL-6), and Interleukin-8 (IL-8) )