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SAB4502581

Sigma-Aldrich

Anti-Retinoic Acid Receptor β, C-Terminal antibody produced in rabbit

affinity isolated antibody

Synonym(s):

HBV-activated protein, RAR-β, RAR-ε, nuclear receptor 1B2, retinoic acid receptor β

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About This Item

MDL number:
MFCD00802879
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 50 kDa

species reactivity

mouse, human

concentration

~1 mg/mL

technique(s)

ELISA: 1:20000
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000

NCBI accession no.

P10826

UniProt accession no.

P10826

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... RARB(5915)

General description

Anti-Retinoic Acid Receptor β Antibody detects endogenous levels of total Retinoic Acid Receptor β protein.
Retinoic Acid Receptor β (RARB) is encoded by the gene mapped to human chromosome 3p24.2-p25. The encoded protein belongs to the nuclear receptor superfamily.

Immunogen

The antiserum was produced against synthesized peptide derived from human Retinoic Acid Receptor beta.

Immunogen Range: 331-380

Biochem/physiol Actions

Retinoic Acid Receptor β (RARB) interacts with its ligand retinoic acid (RA) and retinoid and plays a vital role in normal lung development. It is also involved in growth regulation of mammary epithelial cells. RARB acts as a tumor suppressor protein in various types of cancers, including thyroid carcinomas.
Mutation in the gene is associated with the development of anophthalmia and/or microphthalmia and diaphragmatic hernia. RARβ gene inactivation caused by RARβ methylation contributes to the pathogenesis of non-small cell lung cancer (NSCLC) and acts as a potential biomarker, risk factor and therapeutic target for NSLC.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Physical form

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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.

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Storage Class Code

10 - Combustible liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Elevated retinoic acid receptor β4 protein in human breast tumor cells with nuclear and cytoplasmic localization.
Karen M S, et al.
Proceedings of the National Academy of Sciences of the USA, 96(15), 8651-8656 (1999)
A second locus for Marfan syndrome maps to chromosome 3p24.2-p25.
Gwenaelle C, et al.
Nature Genetics, 8(3), 264-268 (1994)
Association between Retinoic acid receptor-β hypermethylation and NSCLC risk: a meta-analysis and literature review.
Yan L, et al.
Oncotarget, 8(4), 5814?5822-5814?5822 (2017)
K M Sommer et al.
Proceedings of the National Academy of Sciences of the United States of America, 96(15), 8651-8656 (1999-07-21)
The transcription factor retinoic acid receptor beta(2) (RARbeta(2)) is a potent inhibitor of breast cancer cells in vitro, and studies suggest that RARbeta expression is lost in primary breast cancer. Although RARbeta(2) is selectively down-regulated at the mRNA level in
Jingwei Ma et al.
Nature communications, 11(1), 1769-1769 (2020-04-15)
Our current understanding of how sugar metabolism affects inflammatory pathways in macrophages is incomplete. Here, we show that glycogen metabolism is an important event that controls macrophage-mediated inflammatory responses. IFN-γ/LPS treatment stimulates macrophages to synthesize glycogen, which is then channeled
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