GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 04 Sep 2015.
Prostaglandin-endoperoxide synthase 1
cyclooxygenase, COX-1, Cyclooxygenase 1
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 PTGS1, which regulates angiogenesis in endothelial cells, and is inhibited by nonsteroidal anti-inflammatory drugs such as aspirin. PTGS1 is thought to be involved in cell-cell signaling and maintaining tissue homeostasis. Alternative splicing of this gene generates two transcript variants. The expression of these two transcripts is differentially regulated by relevant cytokines and growth factors. [provided by RefSeq, Jul 2008] (from
Kim et al., Seoul, South Korea. In J Periodontol, 03 Oct 2015
Pharmacological and siRNA-mediated inhibition of PLD1 and PLD2 attenuated the nicotine- and LPS-induced upregulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), production of nitric oxide (NO) and prostaglandin E2 (PGE2), and mRNA expression and secretion of tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), and IL-8.
Wood et al., Toronto, Canada. In Prostate, 01 Oct 2015
There was markedly increased inflammatory cell infiltration into the TIMP3-deficient prostate tumors along with increased expression of monocyte chemoattractant protein-1, cyclooxygenase-2, TNF-α, and interleukin-1β; all of which are implicated in inflammation and cancer.
Paulsen et al., Erlangen, Germany. In Exp Eye Res, 01 Oct 2015
Sudan III fat staining, viability and proliferation assays, electric cell-substrate impedance sensing, real-time PCR for gene expression of cyclooxygenase-2 and 15-lipoxygenase and ELISAs for resolvin D1 (RvD1), IFNγ, TNFα and IL-6 were applied.
Lee et al., Taegu, South Korea. In Biomol Ther (seoul), 30 Sep 2015
Biochemical analyses of the IgE/Ag-mediated signaling pathway demonstrated that imperatorin dramatically attenuated degranulation and the production of 5-lipoxygenase-dependent LTC4 and cyclooxygenase-2-dependent PGD2 through the inhibition of intracellular calcium influx/phospholipase Cγ1, cytosolic phospholipase A2/mitogen-activated protein kinases and/or nuclear factor-κB pathways in BMMC.
Cho et al., Chŏnju, South Korea. In Biomol Ther (seoul), 30 Sep 2015
Fisetin diminished the release of nitric oxide (NO) and reduced the mRNA levels of inducible NO synthase (iNOS), tumor necrosis factor (TNF)-α, and cyclooxygenase (COX)-2 in LPS-stimulated RAW264.7 cells without displaying cytotoxicity.
Croubels et al., Merelbeke, Belgium. In Vet Immunol Immunopathol, 15 Sep 2015
Steroidal and nonsteroidal anti-inflammatory drugs ((N)SAIDs) possess anti-inflammatory, antipyretic and analgesic properties through (non)-selective central and peripheral cyclooxygenase (COX) inhibition.
Serhan et al., Boston, United States. In Nat Med, 03 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.
CLINICAL QUESTION: Are nonsteroidal anti-inflammatory drugs (NSAIDs) associated with better outcomes than cyclooxygenase inhibitors, glucocorticoids, IL-1 inhibitors or placebo in the treatment of acute gout?
The interactions between IL-32 and various cytokines including cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS), interferon (IFN)-λ1, interleukin (IL)-6, and soluble IL-6 receptor have been described.
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.
Planas et al., Barcelona, Spain. In J Biol Chem, 2012
Astrocytes respond to lipopolysaccharide by a COX-2-dependent production of prostanoids, mainly vasoactive PGE(2), and suggest that the coordinated down-regulation of COX-1 facilitates PGE(2) production after TLR-4 activation.