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Mouse HPGD / 15-PGDH Protein (His Tag)

15-PGDH, AV026552, MGC14001

Catalog Number P50531-M08E
Organism Species Mouse
Host E. coli
Synonyms 15-PGDH, AV026552, MGC14001
Molecular Weight The recombinant mouse HPGD consisting of 279 amino acids and has a calculated molecular mass of 30.6 kDa. rmHPGD migrates as an approximately 30 kDa band in SDS-PAGE under reducing conditions as predicted.
predicted N Met 1
SDS-PAGE
Purity > 90 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the mouse HPGD (Q8VCC1) (Met 1-Ser 269) was expressed, with a polyhistide tag at the C-terusmin.
Bio-activity Measured by its ability to bind Rhesus ErbB3-His (P 90043-K08H) in functional Elisa.
Research Area Signaling |Signal Transduction |Other Related Intracellular Topics |Cellular Senescence and Pathways in Aging |Apoptosis |Oxidative Stress |
Formulation Lyophilized from sterile PBS, pH 8.0, 20% glycerol
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background 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.
Reference
  • 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.