Mouse prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) ELISA Kit | PTGS2 elisa kit

Mouse cyclooxygenase-2, COX-2 ELISA Kit

Cat. Num. AAA701892

• Gene Names: Ptgs2; COX2; Cox-2; PHS-2; Pghs2; TIS10; PGHS-2
• Reactivity: Mouse
• Synonyms: prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase); Mouse cyclooxygenase-2; COX-2 ELISA Kit; COX-2; COX2; GRIPGHS; PGG/HS; PGHS-2; PHS-2; hCox-2; cyclooxygenase 2b; prostaglandin G/H synthase and cyclooxygenase; prostaglandin-endoperoxide synthase 2; PTGS2 elisa kit

• Reactivity: Mouse
• Specificity: This assay has high sensitivity and excellent specificity for detection of Mouse PTGS2. No significant cross-reactivity or interference between Mouse PTGS2 and analogues was observed.
• Sequence Length: 604

• Samples: Serum, plasma, tissue homogenates
• Detection Range: 78 pg/ml-5000 pg/ml
• Sensitivity: 19.5 pg/ml
• Intra-assay Precision: Intra-assay Precision (Precision within an assay): CV% is less than 8%; Three samples of known concentration were tested twenty times on one plate to assess.; Inter-assay Precision (Precision between assays): CV% is less than 10%; Three samples of known concentration were tested in twenty assays to assess.
• Detection Wavelength: 450 nm
• Sample Volume: 50-100ul
• Protein Biological Process 1: Biosynthesis/Metabolism
• Protein Biological Process 2: Lipogenesis and lipometabolism
• Protein Biological Process 3: Fatty acid biosynthesis
• Preparation and Storage: Unopened test kits should be stored at 2 to 8 degree C upon receipt. Please refer to pdf manual for further storage instructions.

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for PTGS2 elisa kit

Introduction: Cyclooxygenase (COX) is an enzyme (EC 1.14.99.1) that is responsible for formation of important biological mediators called prostanoids, including prostaglandins, prostacyclin and thromboxane. Pharmacological inhibition of COX can provide relief from the symptoms of inflammation and pain. Non-steroidal anti-inflammatory drugs, such as aspirin and ibuprofen, exert their effects through inhibition of COX. The names "prostaglandin synthase (PHS)" and "prostaglandin endoperoxide synthetase (PES)" are still used to refer to COX. At present, three COX isoenzymes are known: COX-1, COX-2, and COX-3. COX-2 is undetectable in most normal tissues. It is an inducible enzyme, becoming abundant in activated macrophages and other cells at sites of inflammation. Selectivity for COX-2 is the main feature of celecoxib, rofecoxib, and other members of this drug class. Because COX-2 is usually specific to inflamed tissue, there is much less gastric irritation associated with COX-2 inhibitors, with a decreased risk of peptic ulceration. The selectivity of COX-2 does not seem to negate other side-effects of NSAIDs, most notably an increased risk of renal failure, and there is evidence that indicates that there might be an increase in the risk for heart attack, thrombosis, and stroke through a increase in thromboxane. The sale of Rofecoxib (brand name Vioxx) was banned in 2004 because of such concerns. Some other COX-2 selective NSAIDs, such as celecoxib, and etoricoxib, are still on the market.

Principle of the Assay: The microtiter plate provided in this kit has been pre-coated with an antibody specific to COX-2. Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody preparation specific for COX-2 and Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. Then a TMB (3,3',5,5' tetramethyl-benzidine) substrate solution is added to each well. Only those wells that contain COX-2, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The concentration of COX-2 in the samples is then determined by comparing the O.D. of the samples to the standard curve.

NCBI and Uniprot Product Information

• NCBI GI #: 31981525
• NCBI GeneID: 19225
• NCBI Accession #: NP_035328.2
• NCBI GenBank Nucleotide #: NM_011198.3
• UniProt Accession #: Q05769; Q543K3
• Molecular Weight: 69,013 Da
• NCBI Official Full Name: prostaglandin G/H synthase 2
• NCBI Official Synonym Full Names: prostaglandin-endoperoxide synthase 2
• NCBI Official Symbol: Ptgs2
• NCBI Official Synonym Symbols: COX2; Cox-2; PHS-2; Pghs2; TIS10; PGHS-2
• NCBI Protein Information: prostaglandin G/H synthase 2; PES-2; PHS II; gripghs; PGH synthase 2; cyclooxygenase 2; cyclooxygenase-2; prostaglandin H2 synthase 2; glucocorticoid-regulated inflammatory cyclooxygenase; macrophage activation-associated marker protein P71/73
• UniProt Protein Name: Prostaglandin G/H synthase 2
• Protein Family: Prostaglandin G/H synthase
• UniProt Gene Name: Ptgs2
• UniProt Synonym Gene Names: Cox-2; Cox2; Pghs-b; Tis10; COX-2; PGH synthase 2; PGHS-2
• UniProt Entry Name: PGH2_MOUSE

Uniprot Description

Function: Converts arachidonate to prostaglandin H2 (PGH2), a committed step in prostanoid synthesis. Constitutively expressed in some tissues in physiological conditions, such as the endothelium, kidney and brain, and in pathological conditions, such as in cancer. PTGS2 is responsible for production of inflammatory prostaglandins. Up-regulation of PTGS2 is also associated with increased cell adhesion, phenotypic changes, resistance to apoptosis and tumor angiogenesis. In cancer cells, PTGS2 is a key step in the production of prostaglandin E2 (PGE2), which plays important roles in modulating motility, proliferation and resistance to apoptosis.5 PublicationsManual assertion based on experiment in:Ref.10

Catalytic activity: Arachidonate + AH2 + 2 O2 = prostaglandin H2 + A + H2O.4 PublicationsManual assertion based on experiment in:Ref.15

Cofactor: Binds 1 heme B (iron-protoporphyrin IX) group per subunit.3 PublicationsManual assertion based on experiment in:Ref.13

Enzyme regulation: Inhibited by the nonsteroidal anti-inflammatory drugs aspirin, naproxen, diclofenac, meclofenamic acid, indomethacin and their analogs.2 PublicationsManual assertion based on experiment in:Ref.15