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MYD88 — PTGS2

Text-mined interactions from Literome

Yeo et al., J Biol Chem 2003 : CpG DNA induced Cox-2 promoter activity was completely inhibited by an endosomal acidification inhibitor ( chloroquine ), a TLR9 antagonist inhibitory CpG DNA, or overexpression of a dominant negative ( DN ) form of MyD88 ... Conclusively, these results demonstrate that endosomal DNA processing and TLR9/MyD88 dependent activation of NF-kappaB and p38 are required for transcriptional regulation of Cox-2 expression induced by CpG DNA, and suggest that interleukin-1 receptor associated kinase and/or TRAF6 may be a diverging point for NF-kappaB activation in response to CpG DNA in RAW264.7 cells
Yeo et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Collectively, our results suggest that MyD88 and MAPKs play a key regulatory role in CpG DNA mediated cox-2 expression at the post-transcriptional level and that TRAF6 is a diverging point in the Toll-like receptor 9-signaling pathway for CpG DNA mediated MAPK activation
Zheng et al., Gastroenterology 2009 (Colitis...) : Exogenous hyaluronic acid induced the expression of tumor necrosis factor alpha, MIP-2, and COX-2 in the colon in a MyD88 dependent manner
Manieri et al., Gastroenterology 2012 : Igf2bp1 expression was induced exclusively in wound bed cMSCs, and full induction of Ptgs2 and Igf2bp1 during repair required Myd88
Månsson et al., Am J Physiol Gastrointest Liver Physiol 2012 (Enterocolitis...) : We noted that cyclooxygenase (Cox)-2 expression was MyD88 dependent , with numerous Cox-2 positive cells identified in fibrotic regions of WT mice at postinfection day 7, but not in MyD88 ( -/- ) mice