WH0000196M2
Monoclonal Anti-AHR antibody produced in mouse
clone 3B12, purified immunoglobulin, buffered aqueous solution
Synonym(s):
Anti-aryl hydrocarbon receptor
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
3B12, monoclonal
form
buffered aqueous solution
species reactivity
human
technique(s)
immunoprecipitation (IP): suitable
indirect ELISA: suitable
indirect immunofluorescence: suitable
western blot: 1-5 μg/mL
isotype
IgG1κ
GenBank accession no.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... AHR(196)
Related Categories
General description
Aryl hydrocarbon receptor (Ahr) is a helix-loop-helix transcription factor and a heterodimeric protein. It is encoded by the gene mapped to human chromosome 7p211. The encoded protein is a member of the helix-loop-helix/Per-Arnt-Sim (bHLH/PAS) family of transcription factors. AHRis mainly expressed in the cytoplasm and is found in a complex with chaperone proteins such as HSP90 (heat shock protein 90), XAP2 (X-associated protein 2 ) and p23 (cochaperone for the Hsp90).
This gene encodes a ligand-activated transcription factor involved in the regulation of biological responses to planar aromatic hydrocarbons. This receptor has been shown to regulate xenobiotic-metabolizing enzymes such as cytochrome P450. Its ligands included a variety of aromatic hydrocarbons. (provided by RefSeq)
Immunogen
AHR (NP_001612, 721 a.a. ~ 820 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Sequence
MGSFEPSPYPTTSSLEDFVTCLQLPENQKHGLNPQSAIITPQTCYAGAVSMYQCQPEPQHTHVGQMQYNPVLPGQQAFLNKFQNGVLNETYPAELNNINN
Sequence
MGSFEPSPYPTTSSLEDFVTCLQLPENQKHGLNPQSAIITPQTCYAGAVSMYQCQPEPQHTHVGQMQYNPVLPGQQAFLNKFQNGVLNETYPAELNNINN
Application
Monoclonal Anti-AHR antibody produced in mouse has been used in western blot technique.
Biochem/physiol Actions
Aryl hydrocarbon receptor (Ahr) helps in the inhibitory effects of 2-(4-hydroxy-3-methoxyphenyl)-benzothiazole (YL-109) on development and invasion of MDA-MB-231 (breast adenocarcinoma cell line) by upregulation of heat shock protein 70 (Hsp70)-interacting protein (CHIP). The encoded protein regulates invasiveness and metastasis of breast cancer cells. Ahr mediates various biological responses to extensive environmental pollutants.
Features and Benefits
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Physical form
Solution in phosphate buffered saline, pH 7.4
Legal Information
GenBank is a registered trademark of United States Department of Health and Human Services
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
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Regulatory Information
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Polycyclic aromatic hydrocarbon components contribute to the mitochondria-antiapoptotic effect of fine particulate matter on human bronchial epithelial cells via the aryl hydrocarbon receptor
Ferecatu I
Particle and Fibre Toxicology (2010)
Human arylhydrocarbon receptor: functional expression and chromosomal assignment to 7p21.
Ema M
Journal of Biochemistry, 116, 845-851 (1994)
Induction of expression of aryl hydrocarbon receptor-dependent genes in human HepaRG cell line modified by shRNA and treated with β-naphthoflavone.
Brauze D
Molecular and Cellular Biochemistry, 425, 59-75 (2017)
Novel Aryl Hydrocarbon Receptor Agonist Suppresses Migration and Invasion of Breast Cancer Cells.
Hanieh H
PLoS ONE, 11 (2016)
Ioana Ferecatu et al.
Particle and fibre toxicology, 7, 18-18 (2010-07-29)
Nowadays, effects of fine particulate matter (PM2.5) are well-documented and related to oxidative stress and pro-inflammatory response. Nevertheless, epidemiological studies show that PM2.5 exposure is correlated with an increase of pulmonary cancers and the remodeling of the airway epithelium involving
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