Anti-HPGD/15-PGDH antibody

Anti-HPGD/15-PGDH antibody

• DataSheet
• Material Safety Data Sheets (MSDS)

Rabbit polyclonal to HPGD/15-PGDH

ELISA, WB, IP

Mouse HPGD / 15-PGDH

15-PGDH antibody; 15-PGDH antibody; AV026552 antibody; Hpgd antibody; HPGD antibody; MGC14001 antibody; PGDH1 antibody; SDR36C1 antibody; PGDH antibody; PGDH antibody; PGDH1 antibody; PHOAR1 antibody; 15-PGDH antibody; SDR36C1 antibody; 15-PGDH antibody; AV026552 antibody

Rabbit IgG

Produced in rabbits immunized with purified, recombinant Mouse HPGD / 15-PGDH (rM HPGD / 15-PGDH; Q8VCC1; Met 1-Ser 269). HPGD / 15-PGDH specific IgG was purified by Mouse HPGD / 15-PGDH affinity chromatography.

Polyclonal

0.2 μm filtered solution in PBS with 5% trehalose

This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

Mouse 15-hydroxyprostaglandin dehydrogenase [NAD+], also known as Prostaglandin dehydrogenase 1, HPGD, and PGDH1, is a member of the short-chain dehydrogenases/reductases (SDR) family. Prostaglandins (PGs) play a key role in the onset of labor in many species and regulate uterine contractility and cervical dilatation. Therefore, the regulation of prostaglandin output by PG synthesizing and metabolizing enzymes in the human myometrium may determine uterine activity patterns in human labor both at preterm and at term. Prostaglandin dehydrogenase (PGDH) metabolizes prostaglandins (PGs) to render them inactive. HPGD is down-regulated by cortisol, dexamethasone and betamethasone and down-regulated in colon cancer. It is up-regulated by TGFB1. HPGD contributes to the regulation of events that are under the control of prostaglandin levels. HPGD catalyzes the NAD-dependent dehydrogenation of lipoxin A4 to form 15-oxo-lipoxin A4. and inhibits in vivo proliferation of colon cancer cells. Defects in HPGD are the cause of primary hypertrophic osteoathropathy autosomal recessive (PHOAR) , cranioosteoarthropathy (COA), and isolated congenital nail clubbing.

• Patel, FA. et al., 2003, J. Clin. Endocrinol. Metab. 88: 2922-33.
• McKeown KJ, et al.,2003, J. Clin. Endocrinol. Metab. 88 (4): 1737-41.
• Yan, M. et al., 2004, Proc. Natl. Acad. Sci. USA. 101: 17468-73.
• Tariq, M. et al., 2009, J Med Genet. 46 (1): 14-20.