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Prostaglandin-endoperoxide synthase 2

Cyclooxygenase 2
Prostaglandin-endoperoxide synthase (PTGS), also known as cyclooxygenase, is the key enzyme in prostaglandin biosynthesis, and acts both as a dioxygenase and as a peroxidase. There are two isozymes of PTGS: a constitutive PTGS1 and an inducible PTGS2, which differ in their regulation of expression and tissue distribution. This gene encodes the inducible isozyme. It is regulated by specific stimulatory events, suggesting that it is responsible for the prostanoid biosynthesis involved in inflammation and mitogenesis. [provided by RefSeq, Feb 2009] (from NCBI)
Top mentioned proteins: cyclooxygenase, V1a, iNOS, Interleukin-6, ACID
Papers on Cyclooxygenase 2
Oral leukoplakia - To treat or not to treat.
Dabelsteen et al., Copenhagen, Denmark. In Oral Dis, Feb 2016
The systemic therapies tested so far include retinoids, extracts of green tea, inhibitors of cyclooxygenase-2 and of epidermal growth factor, and peroxisome proliferator activated receptor-γ agonists (William, 2012), but there is no generally approved standard systemic therapy regimen so far (William, 2012).
Loss of Fatty Acid Binding Protein 4/aP2 Reduces Macrophage Inflammation Through Activation of SIRT3.
Bernlohr et al., Minneapolis, United States. In Mol Endocrinol, Feb 2016
When compared to controls, silencing of SIRT3 in Raw246.7 macrophages leads to increased expression of inflammatory cytokines, inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (Cox2).
Chronic Normobaric Hypoxia Induces Pulmonary Hypertension in Rats: Role of NF-κB.
Gong et al., Wenzhou, China. In High Alt Med Biol, Feb 2016
Lung tissue levels of NF-κB activity, and interleukin (IL)-1β, IL-6, and cyclooxygenase-2 mRNAs, were determined, and mean pulmonary arterial pressure, right ventricular hypertrophy, and right heart function were evaluated.
Therapeutic evaluation of HIV transduction basic domain-conjugated superoxide dismutase solution on suppressive effects of the formation of peroxynitrite and expression of COX-2 in murine skin.
Chen et al., Taipei, Taiwan. In J Biomed Sci, Dec 2015
According to immunohistochemical staining, Tat-SOD successfully suppressed inflammation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), the expression of sodium nitroferricyanide (SNP)-induced cyclooxygenase-2 (COX-2), and the production of nitrotyrosine proteins.
Poly(I:C) increases the expression of mPGES-1 and COX-2 in rat primary microglia.
Fiebich et al., Belo Horizonte, Brazil. In J Neuroinflammation, Dec 2015
METHODS: In the present study, we evaluated the effect of poly(I:C) on the production of prostaglandin E2 (PGE2) and the inducible enzymes cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) in primary rat microglia.
Physiology and pathophysiology of cyclooxygenase-2 and prostaglandin E2 in the kidney.
Frøkiær et al., Århus, Denmark. In Kidney Res Clin Pract, Dec 2015
Since the beginning of 1990s, it has been confirmed that COX exists in 2 isoforms, referred to as COX-1 and COX-2.
Factors affecting platinum sensitivity in cervical cancer.
Fukasawa et al., Tokyo, Japan. In Oncol Lett, Dec 2015
Each specimen was assessed for immunohistochemical expression of Ki-67, p53, B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3, cyclooxygenase-2 (COX-2), and excision repair cross-complementation group 1 (ERCC1).
Coxib's Safety in Patients with Inflammatory Bowel Diseases: A Meta-analysis.
Pellicano et al., Torino, Italy. In Pain Physician, Nov 2015
While the treatment of these rheumatological conditions with traditional non-steroidal anti-inflammatory drugs (NSAIDs) has been reported to lead to frequent IBD exacerbation, the safety of cyclooxygenase-2 (COX-2) inhibitors (Coxibs) remains unclear.
Pancreatic cancer and thromboembolic disease, 150 years after Trousseau.
Andrén-Sandberg et al., Lund, Sweden. In Hepatobiliary Surg Nutr, Oct 2015
The exact pathophysiological mechanisms are still partly understood, but it is known that pancreatic cancer induces a prothrombotic and hypercoagulable state and genetic events involved in neoplastic transformation (e.g., KRAS, c-MET, p53), procoagulant factors [e.g., tissue factor (TF), platelet factor 4 (PF4), plasminogen activator inhibitor type 1 (PAI-1)], mucin production (e.g., through activation of P- and L-selectin) and pro-inflammatory factors [e.g., cytokines, cyclooxygenase-2 (COX-2)] may be implicated.
Elucidation of novel 13-series resolvins that increase with atorvastatin and clear infections.
Serhan et al., Boston, United States. In Nat Med, Sep 2015
Their biosynthesis during neutrophil-endothelial cell interactions was initiated by endothelial cyclooxygenase-2 (COX-2), increased by atorvastatin via S-nitrosylation of COX-2 and reduced by COX-2 inhibitors.
Blocking PGE2-induced tumour repopulation abrogates bladder cancer chemoresistance.
Chan et al., Houston, United States. In Nature, Feb 2015
In vivo administration of the cyclooxygenase-2 (COX2) inhibitor celecoxib effectively abolishes a PGE2- and COX2-mediated wound response gene signature, and attenuates progressive manifestation of chemoresistance in xenograft tumours, including primary xenografts derived from a patient who was resistant to chemotherapy.
Cigarette Smoke Amplifies Inflammatory Response and Atherosclerosis Progression Through Activation of the H1R-TLR2/4-COX2 Axis.
Dileepan et al., Kansas City, United States. In Front Immunol, 2014
Our recent data demonstrated that CS extract enhances histamine- and LPS-induced expression of cyclooxygenase-2 (COX-2) in endothelial cells, suggesting that CS and mast cell mediators may collectively amplify inflammatory response in the vessel wall.
Evaluation of PIK3CA mutation as a predictor of benefit from nonsteroidal anti-inflammatory drug therapy in colorectal cancer.
Midgley et al., London, United Kingdom. In J Clin Oncol, 2014
We sought to determine the predictive utility of PIK3CA mutation for benefit from both cyclooxygenase-2 inhibition and aspirin.
Δ9-THC-caused synaptic and memory impairments are mediated through COX-2 signaling.
Chen et al., New Orleans, United States. In Cell, 2013
Here, we show that synaptic and cognitive impairments following repeated exposure to Δ(9)-tetrahydrocannabinol (Δ(9)-THC) are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that converts arachidonic acid to prostanoids in the brain.
Aspirin use and risk of colorectal cancer according to BRAF mutation status.
Ogino et al., Boston, United States. In Jama, 2013
Experimental evidence implicates a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic cells might be less sensitive to the antitumor effects of aspirin than BRAF-wild-type neoplastic cells.
A novel cytotoxic T lymphocyte epitope analogue with enhanced activity derived from cyclooxygenase-2.
Qi et al., Harbin, China. In Scand J Immunol, 2012
tested the binding affinity and stability of Cyclooxygenase-2 analogues and their ability to elicit specific immune responses
The establishment of supramolecular immunobead real-time PCR and the identification of Cox-2 as a metastasis-related marker in colorectal carcinoma.
Ding et al., Guangzhou, China. In Oncol Rep, 2012
Silencing Cox-2 in vivo reduced the metastastic potential of colorectal cancer.
Overexpression of vasoactive intestinal peptide receptors and cyclooxygenase-2 in human prostate cancer. Analysis of potential prognostic relevance.
Sánchez-Chapado et al., Alcalá de Henares, Spain. In Histol Histopathol, 2012
The overexpression of VPAC1 and VPAC2 receptors and COX-2 in cancer tissue gives them a potential role as targets for diagnosis of prostate cancer.
Meta-analysis of epidemiological studies demonstrates significant association of PTGS2 polymorphism rs689470 and no significant association of rs20417 with prostate cancer.
Li et al., Tianjin, China. In Genet Mol Res, 2011
Meta-analysis of epidemiological studies demonstrates significant association of PTGS2 polymorphism rs689470 and no significant association of rs20417 with prostate cancer.
Rationalization of physico-chemical properties of 5, 6-diarylthiazolo [3,2-b]-1, 2, 4-triazoles towards cyclooxygenase-2 (COX-2) inhibition: a QSAR approach.
Chaturvedi et al., Bhopāl, India. In Indian J Biochem Biophys, 2004
less bulkier, less polar substituents on the parent structure are necessary for better COX-2 inhibitory activity
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