Results 321 to 330 of about 207,862 (335)
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Cyclooxygenase-2 as a therapeutic target
Inflammation Research, 1998Cyclooxygenase (COX)-2 is the predominant COX isoform present at sites of inflammation, and produces prostaglandins (PG) that cause swelling and pain. However, in situations where the release of protective PGs by COX-1 has been lost, the induction of COX-2 may compensate and reduce inflammatory responses.
T. W. Evans, J. A. Mitchell
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Cyclooxygenase‐2 in cancer: A review
Journal of Cellular Physiology, 2018AbstractCyclooxygenase‐2 (COX‐2) is frequently expressed in many types of cancers exerting a pleiotropic and multifaceted role in genesis or promotion of carcinogenesis and cancer cell resistance to chemo‐ and radiotherapy. COX‐2 is released by cancer‐associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and cancer cells to the tumor ...
Nasser Hashemi Goradel +4 more
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Cyclooxygenase-2 selective inhibitors
Drugs of Today, 1999The identification of two cyclooxygenase (COX) enzymes has been a tremendous advance in understanding the role of prostaglandins in inflammation and the actions of nonsteroidal antiinflammatory drugs (NSAIDs). COX-1 activity appears to be related to "constitutive" or "housekeeping" functions in the gastric mucosa, kidney and platelets.
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Cyclooxygenase-2 and kidney failure
Prostaglandins & Other Lipid Mediators, 2012Cyclooxygenase (COX)-dependent prostaglandins are necessary for normal kidney function. These prostaglandins are associated with inflammation, maintenance of sodium and water homeostasis, control of renin release, renal vasodilation, vasoconstriction attenuation, and prenatal renal development.
Ana Maria Gámez-Méndez +3 more
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Cyclooxygenase-2: A Therapeutic Target
Annual Review of Medicine, 2002▪ Abstract Cyclooxygenase (COX), also known as prostaglandin endoperoxide synthase, is the key enzyme required for the conversion of arachidonic acid to prostaglandins. Two COX isoforms have been identified, COX-1 and COX-2. In many situations, the COX-1 enzyme is produced constitutively (e.g., in gastric mucosa), whereas COX-2 is highly inducible (e.
Raymond N. DuBois, Marco Turini
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[Cyclooxygenase 2 and carcinogenesis].
Bulletin du cancer, 2004The membrane glycoprotein Cox2 is regulated at transcriptional and post-transcriptional levels by pro-inflammatory agents, cytokines, growth factors, oncogenes, and tumor-promoters. Cox2 is expressed during early stages of colorectal carcinogenesis from the premalignant adenoma stage, and adenocarcinomas of stomach, colon, breast, lung and prostate ...
Sylvie, Rodrigues +4 more
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Selective inhibition of cyclooxygenase 2
Biochemical Pharmacology, 1994Cyclooxygenase (COX), a key enzyme in the formation of prostanoids, is known to exist in two isoforms: an inducible enzyme (COX 2) and a constitutive from (COX 1). Both enzymes are inhibited by non-steroidal anti-inflammatory drugs (NSAID), but only marginal selectivity has thus far been reported. In this study, we report on a novel selective inhibitor
Volker Ullrich +3 more
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Cyclooxygenase‐2 and Tumor Biology
2007There is now substantial evidence for the role of cyclooxygenase (COX)-2 in causation and prevention of cancer. Selective COX-2 inhibitors (coxibs) were considered attractive candidate chemoprevention agents; however, concerns over the toxicity of systemic selective inhibition have cast some doubt on COX-2 inhibition as a safe chemoprevention strategy.
Shigeru Kanaoka +2 more
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Mediation of Inflammation by Cyclooxygenase-2
1995Non-steroidal antiinflammatory drugs (NSAIDs) are commonly used for the treatment of inflammation, pain, and fever. Mechanistically, these compounds are believed to act via inhibition of the enzyme cyclooxygenase (COX), which catalyzes the conversion of arachidonic acid to the prostaglandins (PGs). Although commercially available NSAIDS are efficacious
Yan Zhang +8 more
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Cyclooxygenase-2 and Nitric Oxide
Journal of Cardiovascular Pharmacology, 2006Nitric oxide (NO) is a simple but pluripotent molecule that is mainly released from vascular endothelial cells where it is formed intracellularly by nitric oxide synthase from L-arginine in response to several stimuli, including shear stress or muscarinic receptor stimulation. NO stimulates guanylyl cyclase to form cyclic guanosine monophosphate, which
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