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HPGD / 15-PGDH Antibody (FITC), Rabbit MAb

  • HPGD / 15-PGDH Antibody (FITC), Rabbit MAb, Flow cytometric
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Human HPGD Antibody Product Information
Immunogen:Recombinant Human HPGD / 15-PGDH protein (Catalog#11205-H08E)
Clone ID:027
Ig Type:Rabbit IgG
Concentration:5 μl/Test, 0.1 mg/ml
Formulation:Aqueous solution containing 0.5% BSA and 0.09% sodium azide
Preparation:This antibody was obtained from a rabbit immunized with purified, recombinant Human HPGD / 15-PGDH (rh HPGD / 15-PGDH; Catalog#11205-H08E; NP_000851.2; Met1-Gln266) and conjugated with FITC under optimum conditions, the unreacted FITC was removed.
Human HPGD Antibody Usage Guide
Specificity:Human HPGD / 15-PGDH
Application:FCM
Storage:
Human HPGD Antibody FC Application Image
HPGD / 15-PGDH Antibody (FITC), Rabbit MAb, Flow cytometric
[Click to enlarge image]
Caption:
Human HPGD expression in Jurkat cells.
Other HPGD Antibody Products
Immunochemical staining of human CCNF in human brain with rabbit polyclonal antibody (1 µg/mL, formalin-fixed paraffin embedded sections).
HPGD/15-PGDH Background

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.

Human HPGD/15-PGDH References
  • 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.
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    Catalog: 11205-R027-F-25
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    Datasheet & Documentation

    All information of our products is subject to change without notice. Please refer to COA enclosed in shipped package for the newest information.
    Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"