Gene interactions and pathways from curated databases and text-mining

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APOB — PTGS2

Text-mined interactions from Literome

Pontsler et al., J Biol Chem 2002 : These cells express cyclooxygenase-2, but the way oxidized LDL stimulates cyclooxygenase-2 transcription is unknown
Norata et al., Int J Mol Med 2004 : N-LDL and Ox-LDL induced Cox-2 expression in a time- and dose dependent manner ... N-LDL and Ox-LDL increased PGE2 release in a Cox-2 dependent manner while TXA2 and PGI2 release were not affected either by n-LDL or Ox-LDL ... The finding that n-LDL and Ox-LDL induces Cox-2 in human endothelial cells through a p38 MAPK, NF-kappaB, CREB dependent pathway thus modulating PGE2 release, suggests a new mechanism by which these lipoproteins induce endothelial dysfunction, sustaining inflammatory processes in the arterial wall
Kanayama et al., J Biol Chem 2007 : In the present study, based on the finding that HNE induced COX-2 expression only in the serum containing media, we characterized a serum component essential for the HNE induced COX-2 induction and found that low density lipoprotein (LDL) that had been denatured by freeze thawing or oxidized LDL might be involved in the COX-2 induction
Taketa et al., J Biol Chem 2008 (Atherosclerosis...) : Ox-LDL transiently induced cyclooxygenase-2 (COX-2) mRNA and protein expression, and COX-2 specific inhibition by NS-398 or meloxicam or small interference RNA of COX-2 suppressed Ox-LDL induced PPARalpha and PPARgamma activation ... On the other hand, Ox-LDL increased intracellular 15-deoxy-Delta ( 12,14 ) -prostaglandin J ( 2 ) ( 15d-PGJ ( 2 ) ) level through ERK1/2 dependent overexpression of COX-2 ... Ox-LDL induced phosphorylation of ERK1/2 and p38 MAPK, and ERK1/2 specific inhibition abrogated Ox-LDL induced COX-2 expression and PPARalpha and PPARgamma activation, whereas p38 MAPK-specific inhibition had no effect
Zhao et al., J Cardiovasc Pharmacol 2008 : The results showed that aspirin significantly suppressed COX-2 and ICAM-1 expression induced by ox-LDL and also inhibited IkappaB phosphorylation in human umbilical vein endothelial cells ( HUVECs )