Anti-COX2/Cyclooxygenase 2/PTGS2 Antibody Picoband® Fluoro647 Conjugated

Cyclooxygenase (Cox) is the key enzyme in conversion of arachidonic acid to PGs, and two isoforms, Cox-1 and Cox-2, have been identified. Cox-2 gene encodes an inducible prostaglandin synthase enzyme that is overexpressed in adenocarcinomas and other tumors. Deletion of the murine Cox-2 gene in Min mice reduced the incidence of intestinal tumors, suggesting that it is required for tumorigenesis. This gene is localized to sites associated with retinal blood vessels, and plays an important role in blood vessel formation in the retina. And the glucocorticoid receptor suppression of COX-2 is also crucial for curtailing lethal immune activation, and suggest new therapeutic approaches for regulation of T-cell-mediated inflammatory diseases.

Prostaglandin G/H synthase 2;1.14.99.1; Cyclooxygenase-2; COX-2; PHS II; Prostaglandin H2 synthase 2; PGH synthase 2; PGHS-2; Prostaglandin-endoperoxide synthase 2; PTGS2; COX2

Atherosclerosis, Cancer, Cancer Metabolism, Cardiovascular, Cholesterol Metabolism, Endocrine Metabolism, Heart Disease, Hormone Biosynthesis, Lipid and Lipoprotein Metabolism, Lipid Metabolism, Lipid Signaling, Lipids/Lipoproteins, Metabolic Signaling Pathway, Metabolic Signaling Pathways, Metabolism, Pathways and Processes, Platelets, Signal Transduction, Signaling Pathway, Tumor Biomarkers

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. .

1. Salmenkivi, K.; Haglund, C.; Ristimaki, A.; Arola, J.; Heikkila, P. : Increased expression of cyclooxygenase-2 in malignant pheochromocytomas. J. Clin. Endocr. Metab. 86: 5615-5619, 2001. 2. Liu, C. H.; Chang, S.-H.; Narko, K.; Trifan, O. C.; Wu, M.-T.; Smith, E.; Haudenschild, C.; Lane, T. F.; Hla, T. : Overexpression of cyclooxygenase-2 is sufficient to induce tumorigenesis in transgenic mice. J. Biol. Chem. 276: 18563-18569, 2001. 3. Wilkinson-Berka, J. L.; Alousis, N. S.; Kelly, D. J.; Gilbert, R. E. : COX-2 inhibition and retinal angiogenesis in a mouse model of retinopathy of prematurity. Invest. Ophthal. Vis. Sci. 44: 974-979, 2003. 4. Brewer, J. A.; Khor, B.; Vogt, S. K.; Muglia, L. M.; Fujiwara, H.; Haegele, K. E.; Sleckman, B. P.; Muglia, L. J. : T-cell glucocorticoid receptor is required to suppress COX-2-mediated lethal immune activation. Nature Med. 9: 1318-1322, 2003.