Anti-Seladin-1 (C-terminal) antibody produced in rabbit

enhanced validation

IgG fraction of antiserum, buffered aqueous solution

Anti-24-dehydro-cholesterol reductase (DCHR24), Diminuto/Dwarf-1 homolog, Anti-Selective Alzheimer’s Disease Indicator-1
MDL number:
Pricing and availability is not currently available.

biological source


antibody form

IgG fraction of antiserum

antibody product type

primary antibodies




buffered aqueous solution

mol wt

antigen ~60 kDa

species reactivity


enhanced validation

recombinant expression
Learn more about Antibody Enhanced Validation


western blot: 1:1,000-1:2,000 using HEK293 cells expressing human seladin-1.



UniProt accession no.

shipped in

dry ice

storage temp.


Gene Information

human ... DYNC1I2(1781)

General description

Selective Alzheimer′s disease indicator-1 (seladin-1) protein is encoded by the 3-β-hydroxysterol-24-reductase (DHCR24) gene. This protein is mainly located in the endoplasmic reticulum. Seladin-1 contains a highly conserved flavin adenine dinucleotide (FAD)-binding domain. DHCR24 gene is located on human chromosome 1p32.3. This gene contains 8 introns and 9 exons.


Anti-Seladin-1(C-terminal) recognizes human seladin-1.


synthetic peptide corresponding to amino acids 505-516 located in a region near the C-terminus of human seladin-1.


Anti-Seladin-1 (C-terminal) antibody produced in rabbit may be used in immunoblotting.

Biochem/physiol Actions

Selective Alzheimer′s disease indicator-1 (seladin-1) protein catalyzes the conversion of desmosterol to cholesterol. It can protect neurons from β-amyloid toxicity and oxidative stress. In addition, it prevents apoptosis via inhibition of caspase-3, stating that seladin-1 may be involved in the regulation of cell survival and death. Seladin-1 aids to mediate Ras-induced senescence in mouse and human fibroblasts. This protein is upregulated in adrenocortical adenomas and in some tumors. DHCR24 participates plays a key role in cell differentiation, antiapoptotic function, and anti-inflammatory activity. Seladin-1 is known to involve in cholesterol biosynthesis l. A defect in DHCR24 enzyme results in desmosterolosis.

Target description

Seladin-1 (C-terminal) is an anti-apoptotic gene, found to be down regulated in large pyramidal neurons in brain regions affected by AD, and to be involved in the regulation of cellular response tooncogenic and oxidative stress.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, and containing 15 mM sodium azide.

Storage and Stability

For extended storage, freeze in working aliquots at –20 °C. Repeated freezing and thawing, or storage in "frost-free" freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilution samples should be discarded if not used within 12 hours. For continuous use, store at 2-8 °C for up to one month.


Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Personal Protective Equipment

dust mask type N95 (US),Eyeshields,Gloves


NONH for all modes of transport

WGK Germany


Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Desmosterolosis presenting with multiple congenital anomalies
Rohanizadegan M and Sacharow S
European Journal of Medical Genetics, 61(3), 152-156 (2018)
DHCR24 predicts poor clinicopathological features of patients with bladder cancer: A STROBE-compliant study
Liu XP, et al.
Medicine, 97(39) (2018)
Regulation of cellular response to oncogenic and oxidative stress by Seladin-1
Wu C, et al.
Nature, 432(2), 640-645 (2004)
DHCR24 associates strongly with the endoplasmic reticulum beyond predicted membrane domains: implications for the activities of this multi-functional enzyme
Zerenturk EJ, et al.
Bioscience Reports, 34(2), 152-156 (2014)

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