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DHCR7 Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IF |
|---|---|
| Primary Accession | Q9UBM7 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | H=54;M=54 KDa |
| Isotype | Rabbit IgG |
| Antigen Source | HUMAN |
| Gene ID | 1717 |
|---|---|
| Antigen Region | 437-463 aa |
| Other Names | 7-dehydrocholesterol reductase, 7-DHC reductase, Putative sterol reductase SR-2, Sterol Delta(7)-reductase, DHCR7, D7SR |
| Dilution | IF~~1:25 WB~~1:2000 |
| Target/Specificity | This DHCR7 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 437-463 amino acids from the C-terminal region of human DHCR7. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | DHCR7 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | DHCR7 |
|---|---|
| Synonyms | D7SR |
| Function | 7-dehydrocholesterol reductase of the cholesterol biosynthetic pathway reducing the C7-C8 double bond of cholesta-5,7- dien-3beta-ol (7-dehydrocholesterol/7-DHC) and cholesta-5,7,24-trien- 3beta-ol, two intermediates in that pathway. |
| Cellular Location | Endoplasmic reticulum membrane; Multi-pass membrane protein |
| Tissue Location | Widely expressed. Most abundant in adrenal gland, liver, testis, and brain. |
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Provided below are standard protocols that you may find useful for product applications.
Background
This gene encodes an enzyme that removes the C(7-8) double bond in the B ring of sterols and catalyzes the conversion of 7-dehydrocholesterol to cholesterol. This gene is ubiquitously expressed and its transmembrane protein localizes to the endoplasmic reticulum membrane and nuclear outer membrane. Mutations in this gene cause Smith-Lemli-Opitz syndrome (SLOS); a syndrome that is metabolically characterized by reduced serum cholesterol levels and elevated serum 7-dehydrocholesterol levels and phenotypically characterized by mental retardation, facial dysmorphism, syndactyly of second and third toes, and holoprosencephaly in severe cases to minimal physical abnormalities and near-normal intelligence in mild cases. Alternative splicing results in multiple transcript variants that encode the same protein.
References
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)
Koo, G., et al. Am. J. Med. Genet. A 152A (8), 2094-2098 (2010) :
Wang, T.J., et al. Lancet 376(9736):180-188(2010)
Ahn, J., et al. Hum. Mol. Genet. 19(13):2739-2745(2010)
Jugessur, A., et al. PLoS ONE 5 (7), E11493 (2010) :
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