SAB4502581
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
biological source
rabbit
Quality Level
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.
UniProt accession no.
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
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.
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
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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
Regulatory Information
常规特殊物品
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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)
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)
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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