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MABS1988

Sigma-Aldrich

Anti-SREBP-2 Antibody, clone 22D5

clone 22D5, from rabbit

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Synonym(s):
Sterol regulatory element-binding protein 2, SREBP2, Sterol regulatory element-binding transcription factor 2
eCl@ss:
32160702

biological source

rabbit

Quality Level

antibody form

unpurified

antibody product type

primary antibodies

clone

22D5, monoclonal

species reactivity

mouse, human

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

ambient

target post-translational modification

unmodified

Gene Information

human ... SREBF2(6721)
mouse ... Srebf2(20788)

General description

Sterol regulatory element-binding protein 2 (UniProt: Q3U1N2; also known as SREBP-2, Sterol regulatory element-binding transcription factor 2) is encoded by the Srebf2 (also known as Srebp2) gene (Gene ID: 20788) in murine species. SREBPs are a family of transcription factors that regulate lipid homeostasis by controlling the expression of a range of enzymes that are required for endogenous cholesterol, fatty acid, triacylglycerol, and phospholipid synthesis. The three SREBP isoforms known as, SREBP-1a, SREBP-1c, and SREBP-2, have different roles in lipid synthesis. SREBP-1 and SREBP-2 proteins share 47% of homology. SREBP-2 is mainly involved in cholesterol synthesis and SREBP-1c is mainly involved in fatty acid synthesis and insulin induced glucose metabolism and SREBP-1a isoform is involved in both of these pathways. SREBPs are synthetized as inactive precursor proteins that are bound to the endoplasmic reticulum membranes and upon activation, the precursor is cleaved off in a two-step process to release the N-terminal active domain in the nucleus. SREBP precursors are organized into three domains - an N-terminal domain that contains the transactivation domain, a region rich in serine and proline, and the bHLH-LZ region for DNA binding and dimerization. Sterols are shown to inhibit the cleavage of the precursor protein and the mature nuclear form is rapidly catabolized, thereby reducing transcription. It regulates transcription of the LDL receptor gene as well as the cholesterol and to a lesser degree the fatty acid synthesis pathway. It binds the sterol regulatory element 1 (SRE-1) (5′-ATCACCCCAC-3′) found in the flanking region of the LDRL and HMG-CoA synthase genes. The hepatic overexpression of SREBP-2 isoform in mice causes a preferential induction of genes involved in cholesterol biosynthesis. (Ref.: Eberle, D et al. (2004) Biochimie 86(11); 839-48).

Specificity

Clone 22D5 specifically detected Sterol regulatory element-binding protein 2. It targets an epitope within the 219 amino acids from the N-terminal region.

Immunogen

His-tagged recombinant fragment corresponding to 219 amino acids from the N-terminal region of murine Sterol regulatory element-binding protein 2.

Application

Anti-SREBP-2, clone 22D5, Cat. No. MAB1988, a rabbit monoclonal antibody detects murine SREBP-2 by Western Blotting.
Research Category
Signaling
Western Blotting Analysis: A 1:1,000 dilution from a representative lot detected SREBP-2 in 10 µg of HEK293 and HeLa cell lysates.

Western Blotting Analysis: A representative lot detected SREBP-2 in Western Blotting applications (McFarlane, M.R., et. al. (2015). J Lipid Res. 56(8):1560-71).

Quality

Evaluated by Western Blotting in HepG2 cell lysate.

Western Blotting Analysis: A 1:1,000 dilution of this antibody detected SREBP-2 in 10 µg of HepG2 cell lysate.

Target description

~122 kDa observed; 122.91 kDa calculated. ncharacterized bands may be observed in some lysate(s).

Physical form

Format: Unpurified
Rabbit monoclonal antibody in cell culture supernatant without azide.
Unpurified

Storage and Stability

Stable for 1 year at -20°C from date of receipt.

Handling Recommendations: Upon receipt and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.

Other Notes

Concentration: Please refer to lot specific datasheet.

Disclaimer

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.

Storage Class

10 - Combustible liquids

wgk_germany

WGK 1


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Nityanand Bolshette et al.
PLoS biology, 21(11), e3002367-e3002367 (2023-11-15)
In mammals, O2 and CO2 levels are tightly regulated and are altered under various pathological conditions. While the molecular mechanisms that participate in O2 sensing are well characterized, little is known regarding the signaling pathways that participate in CO2 signaling
Bo Wang et al.
Cell stem cell, 22(2), 206-220 (2018-02-06)
Adequate availability of cellular building blocks, including lipids, is a prerequisite for cellular proliferation, but excess dietary lipids are linked to increased cancer risk. Despite these connections, specific regulatory relationships between membrane composition, intestinal stem cell (ISC) proliferation, and tumorigenesis
Li Zhang et al.
eLife, 6 (2017-10-27)
Cholesterol homeostasis is maintained through concerted action of the SREBPs and LXRs. Here, we report that RNF145, a previously uncharacterized ER membrane ubiquitin ligase, participates in crosstalk between these critical signaling pathways. RNF145 expression is induced in response to LXR
Shiqian Han et al.
iScience, 26(5), 106613-106613 (2023-05-02)
Niemann-Pick disease type C (NP-C) is a genetic lysosomal disorder associated with progressive neurodegenerative phenotypes. Its therapeutic options are very limited. Here, we show that lithium treatment improves ataxia and feeding phenotypes, attenuates cerebellar inflammation and degeneration, and extends survival
Antwi-Boasiako Oteng et al.
Molecular nutrition & food research, 63(19), e1900385-e1900385 (2019-07-22)
The mechanisms underlying the deleterious effects of trans fatty acids on plasma cholesterol and non-alcoholic fatty liver disease (NAFLD) are unclear. Here, the aim is to investigate the molecular mechanisms of action of industrial trans fatty acids. Hepa1-6 hepatoma cells

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