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PTGS2 — TNFSF11

Text-mined interactions from Literome

Kotake et al., J Clin Invest 1999 (Arthritis, Rheumatoid) : These findings suggest that IL-17 first acts on osteoblasts, which stimulates both COX-2 dependent PGE2 synthesis and ODF gene expression, which in turn induce differentiation of osteoclast progenitors into mature osteoclasts, and that IL-17 is a crucial cytokine for osteoclastic bone resorption in RA patients
Chikazu et al., J Bone Miner Res 2001 : We conclude that FGF-2 regulates osteoclast differentiation through two different mechanisms : ( 1 ) an indirect stimulatory action via osteoblasts to induce RANKL/ODF partly through COX-2 induction and prostaglandin production and ( 2 ) a direct inhibitory action on osteoclast precursors by counteracting M-CSF signaling
Han et al., Blood 2005 : Among identified targets, we show that RANKL selectively induces cyclooxygenase (COX) 2 expression via Rac1 that results in turn in production of prostaglandin E2 ( PGE2 ) in RAW 264.7 cells
Wei et al., J Bone Miner Res 2005 (Bone Resorption) : Fibroblasts express RANKL and support osteoclastogenesis in a COX-2 dependent manner after stimulation with titanium particles
Kaneko et al., Prostaglandins Leukot Essent Fatty Acids 2007 : RANKL and PGE2 produced small, additive increases in COX-2 mRNA levels, while LPS produced a larger increase ... We conclude that RANKL stimulated osteoclastogenesis can be enhanced by PGE2 and LPS though direct effects on the hematopoietic cell lineage and that these effects may be mediated in part by induction of COX-2 and enhanced intracellular PG production
Sanuki et al., Connect Tissue Res 2010 : As CF increased, PGE ( 2 ) production and the expression of COX-2 , M-CSF, and RANKL increased , whereas OPG expression decreased ... Celecoxib, a specific inhibitor of COX-2 , blocked the stimulatory effect of CF on TRAP staining and the production of PGE ( 2 ), M-CSF, RANKL , and OPG
Zheng et al., Biol Pharm Bull 2013 : CPC also inhibited RANKL induced activation of extracellular signal regulated kinase ( ERK ) and NF-?B and expression of cyclooxygenase (COX)-2