Product Pathways - Metabolism
DHCR24/Seladin-1 (C59D8) Rabbit mAb #2033
|W IP IHC-P||H M||Endogenous||54||Rabbit IgG|
Reactivity Key: H=Human M=Mouse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
DHCR24/Seladin-1 (C59D8) Rabbit mAb detects endogenous levels of total DHCR24/Seladin-1 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to the sequence of human DHCR24/Seladin-1.
DHCR24/Seladin-1 was identified as a molecular basis for desmosterolosis (1). It encodes for 24-dehydrocholesterol reductase (3β-hydroxysterol Δ-24-reductase). This enzyme reduces desmosterol in cholesterol biosynthesis (1). Recessive mutations in this gene in desmosterolosis patients lead to a defective enzyme resulting in increased levels of desmosterol (1). DHCR24/Seladin-1 is induced upon oxidative stress and was found to mediate Ras-induced senescence resulting from increased reactive oxygen species (2). Studies further indicate that the level of DHCR24/Seladin-1 is induced in the acute response and reduced in the chronic response to oxidative stress in a cholesterol dependent manner (3). Moreover, overexpression of DHCR24/Seladin-1 bearing two mutations that abolish its reductase acitivity causes the cells to lose protection from oxidative stress (3). These findings thus link the reductase activity of DHCR24/Seladin-1 to its protective role in oxidative stress. This enzyme has also been demonstrated to be a hydrogen peroxide scavenger (4).
- Waterham, H.R. et al. (2001) Am J Hum Genet 69, 685-94.
- Wu, C. et al. (2004) Nature 432, 640-5.
- Kuehnle, K. et al. (2008) Mol Cell Biol 28, 539-50.
- Lu, X. et al. (2008) Endocrinology 149, 3267-73.
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For Research Use Only. Not For Use In Diagnostic Procedures.