Gene interactions and pathways from curated databases and text-mining

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PTGS2 — SOD1

Text-mined interactions from Literome

Fang et al., J Neurochem 2000 : Although AdCu/ZnSOD and AdMnSOD infection increased the expression of superoxide dismutase proteins, COX-2 expression was not induced
Armstead et al., Anesthesiology 2003 (Brain Injuries) : Indomethacin ( a cyclooxygenase-1 and cyclooxygenase-2 inhibitor ), NS398 ( a cyclooxygenase-2 inhibitor ), and polyethylene glycol superoxide dismutase and catalase ( free radical scavengers ) partially restored impaired mastoparan dilation after FPI in the newborn in a roughly equivalent manner but not in the juvenile ( 3 +/- 1 and 5 +/- 1 vs. 8 +/- 1 and 13 +/- 1 % newborn, 6 +/- 1 and 9 +/- 1 vs. 7 +/- 1 and 10 +/- 1 % juvenile for NS398 pretreatment )
Maihöfner et al., Eur J Neurosci 2003 (Amyotrophic Lateral Sclerosis) : However, to determine the exact role of COX-2 in human ALS will require further research
Kiritoshi et al., Diabetes 2003 (Diabetes Mellitus, Experimental...) : Similarly, incubation of HMCs with 30 mmol/l glucose significantly increased mitochondrial membrane potential, intracellular ROS production, COX-2 protein expression, and PGE2 synthesis, and these events were completely suppressed by thenoyltrifluoroacetone or carbonyl cyanide m-chlorophenylhydrazone, inhibitors of mitochondrial metabolism, or by overexpression of uncoupling protein-1 or manganese superoxide dismutase
Lee et al., Exp Mol Med 2009 : Differential regulation of inducible nitric oxide synthase and cyclooxygenase-2 expression by superoxide dismutase in lipopolysaccharide stimulated RAW 264.7 cells ... These data suggest that SOD differentially regulate expression of iNOS and COX-2 in LPS stimulated RAW 264.7 cells
Tamura et al., J Clin Endocrinol Metab 2011 : Progesterone inhibited COX-2 expression by inhibiting the binding of NF-?B to its response element but did not inhibit TNFa induced Mn-SOD expression
Sharma-Walia et al., Oncogenesis 2012 : We demonstrate that COX-2 inhibition, via its chemical inhibitors ( NS-398 or celecoxib ), reduced v-FLIP/K13 mediated NF-?B induction, and extracellular matrix ( ECM ) interaction mediated signaling, mitochondrial antioxidant enzyme manganese superoxide dismutase ( MnSOD ) levels, and subsequently downregulated detachment induced apoptosis ( anoikis ) resistance