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anti-AR antibody :: Rabbit Androgen Receptor (AR) Antibody

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Catalog # MBS462010
Unit / Price
  0.1 mg  /  $245 +1 FREE 8GB USB
Testing Data
Product Name

Androgen Receptor (AR), Antibody

Full Product Name

Rabbit anti AR antibody

Product Synonym Names
Rabbit anti-AR (NT); Androgen Receptor; Dihydrotestosterone Receptor
Product Gene Name
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
Chromosome Location
Chromosome: X; NC_000023.10 (66763874..66944119). Location: Xq12
OMIM
300068
3D Structure
ModBase 3D Structure for P10275
Host
Rabbit
Species Reactivity
Human, Rat, Mouse, Canine
Specificity
This antibody recognizes ~110 kDa of human AR protein. It also reacts with mouse and rat. The other species are not tested.
Purity/Purification
The Rabbit IgG is purified by Site-specific Epitope Affinity Purification.
Form/Format
This affinity purified antibody is supplied in sterile Tris-buffered saline (pH7.2) containing antibody stabilizer
Concentration
Size: 100 ug/200 ul (lot specific)
Antigen Preparation
A synthetic peptide corresponding to N-term of human AR. This sequence is identical among human, rat, mouse, dog.
Positive Control
LNCaP prostate Ca Cell
Cellular Location
Nuclear
Preparation and Storage
The antibodies are stable for 12 months from date of receipt when stored at -20 degree C to -70 degree C. The antibodies can be stored at 2 degree C-8 degree C for three month without detectable loss of activity. Avoid repeated freezing-thawing cycles.
Other Notes
Small volumes of anti-AR antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.
Related Product Information for
anti-AR antibody
The androgen receptor (AR), a member of nuclear receptor family, is essential for the growth of prostate cancer cells. The phosphorylation of AR is induced by growth factors and elevated in hormone-refractory prostate tumors. It's been reported the signal pathway of the PI3K/AKT, Src to be responsible for phosphorylation of AR at Ser213/210 and Ser81. The abnormal activation of AR is observed in many diseases, such as prostate cancer.
Applications Tested/Suitable for anti-AR antibody
ELISA, Western Blot, Immunohistochemistry
Application Notes for anti-AR antibody
Western Blot: 0.1-1 ug/ml
ELISA: 0.01-0.1 ug/ml
Immunoprecipitation: 2-5 ug/ml
Immunohistochemistry: 2-5 ug/ml

Testing Data of anti-AR antibody
anti-AR antibody Testing Data image
NCBI/Uniprot data below describe general gene information for AR. It may not necessarily be applicable to this product.
NCBI GI #
NCBI GeneID
UniProt Primary Accession #
UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
110 kDa
NCBI Official Full Name
androgen receptor
NCBI Official Synonym Full Names
androgen receptor
NCBI Official Symbol
NCBI Official Synonym Symbols
KD; AIS; TFM; DHTR; SBMA; HYSP1; NR3C4; SMAX1; HUMARA
  [Similar Products]
NCBI Protein Information
androgen receptor; OTTHUMP00000023450; OTTHUMP00000217211; dihydrotestosterone receptor; androgen nuclear receptor variant 2; nuclear receptor subfamily 3 group C member 4
UniProt Protein Name
Androgen receptor
UniProt Synonym Protein Names
Dihydrotestosterone receptor; Nuclear receptor subfamily 3 group C member 4
Protein Family
UniProt Gene Name
UniProt Synonym Gene Names
DHTR; NR3C4  [Similar Products]
UniProt Entry Name
ANDR_HUMAN
NCBI Summary for AR
The androgen receptor gene is more than 90 kb long and codes for a protein that has 3 major functional domains: the N-terminal domain, DNA-binding domain, and androgen-binding domain. The protein functions as a steroid-hormone activated transcription factor. Upon binding the hormone ligand, the receptor dissociates from accessory proteins, translocates into the nucleus, dimerizes, and then stimulates transcription of androgen responsive genes. This gene contains 2 polymorphic trinucleotide repeat segments that encode polyglutamine and polyglycine tracts in the N-terminal transactivation domain of its protein. Expansion of the polyglutamine tract causes spinal bulbar muscular atrophy (Kennedy disease). Mutations in this gene are also associated with complete androgen insensitivity (CAIS). Two alternatively spliced variants encoding distinct isoforms have been described. [provided by RefSeq]
UniProt Comments for AR
Function: Steroid hormone receptors are ligand-activated transcription factors that regulate eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Transcription factor activity is modulated by bound coactivator and corepressor proteins. Transcription activation is down-regulated by NR0B2. Activated, but not phosphorylated, by HIPK3. Ref.33 Ref.44 Ref.51 Ref.56 Ref.58

Enzyme regulation: AIM-100 (4-amino-5,6-biaryl-furo[2,3-d]pyrimidine) suppresses TNK2-mediated phosphorylation at Tyr-267. Inhibits the binding of the Tyr-267 phosphorylated form to androgen-responsive enhancers (AREs) and its transcriptional activity. Ref.47

Subunit structure: Binds DNA as a homodimer. Part of a ternary complex containing AR, EFCAB6/DJBP and PARK7. Interacts with HIPK3 and NR0B2 in the presence of androgen. The ligand binding domain interacts with MYST2/HBO1 in the presence of dihydrotestosterone. Interacts with EFCAB6/DJBP, PELP1, PQBP1, RANBP9, RBAK, SPDEF, SRA1, TGFB1I1, ZNF318 and RREB1. Interacts with ZMIZ1/ZIMP10 and ZMIZ2/ZMIP7 which both enhance its transactivation activity. Interacts with SLC30A9 and RAD54L2/ARIP4

By similarity. Interacts via the ligand-binding domain with LXXLL and FXXLF motifs from NCOA1, NCOA2, NCOA3, NCOA4 and MAGEA11. The AR N-terminal poly-Gln region binds Ran resulting in enhancement of AR-mediated transactivation. Ran-binding decreases as the poly-Gln length increases. Interacts with HIP1 (via coiled coil domain). Interacts (via ligand-binding domain) with TRIM68. Interacts with TNK2. Interacts with USP26. Interacts with RNF6. Interacts (regulated by RNF6 probably through polyubiquitination) with RNF14; regulates AR transcriptional activity. Interacts with PRMT2 and TRIM24. Interacts with GNB2L1/RACK1. Ref.22 Ref.23 Ref.24 Ref.25 Ref.26 Ref.27 Ref.29 Ref.30 Ref.31 Ref.32 Ref.33 Ref.34 Ref.35 Ref.36 Ref.39 Ref.40 Ref.41 Ref.42 Ref.43 Ref.44 Ref.46 Ref.50 Ref.51 Ref.56 Ref.58

Subcellular location: Nucleus. Cytoplasm. Note: Predominantly cytoplasmic in unliganded form but translocates to the nucleus upon ligand-binding. Can also translocate to the nucleus in unliganded form in the presence of GNB2L1. Ref.7 Ref.32 Ref.39 Ref.44

Tissue specificity: Isoform 2 is mainly expressed in heart and skeletal muscle. Ref.7

Domain: Composed of three domains: a modulating N-terminal domain, a DNA-binding domain and a C-terminal ligand-binding domain. In the presence of bound steroid the ligand-binding domain interacts with the N-terminal modulating domain, and thereby activates AR transcription factor activity. Agonist binding is required for dimerization and binding to target DNA. The transcription factor activity of the complex formed by ligand-activated AR and DNA is modulated by interactions with coactivator and corepressor proteins. Interaction with RANBP9 is mediated by both the N-terminal domain and the DNA-binding domain. Interaction with EFCAB6/DJBP is mediated by the DNA-binding domain. Ref.50 Ref.56

Post-translational modification: Sumoylated on Lys-386 (major) and Lys-520. Ubiquitinated. Deubiquitinated by USP26. 'Lys-6' and 'Lys-27'-linked polyubiquitination by RNF6 modulates AR transcriptional activity and specificity. Ref.44 Ref.46Phosphorylated in prostate cancer cells in response to several growth factors including EGF. Phosphorylation is induced by c-Src kinase (CSK). Tyr-534 is one of the major phosphorylation sites and an increase in phosphorylation and Src kinase activity is associated with prostate cancer progression. Phosphorylation by TNK2 enhances the DNA-binding and transcriptional activity and may be responsible for androgen-independent progression of prostate cancer. Ref.37 Ref.41 Ref.45 Ref.47

Polymorphism: The poly-Gln region of AR is highly polymorphic and the number of Gln varies in the population (from 17 to 26). A smaller size of the poly-Gln region may be associated with the development of prostate cancer.The poly-Gly region of AR is polymorphic and ranges from 24 to 31 Gly. A poly-Gly region shorter or equal to 23 may be associated with the development of androgenetic alopecia.

Involvement in disease: Defects in AR are the cause of androgen insensitivity syndrome (AIS) [

MIM:300068]; previously known as testicular feminization syndrome (TFM). AIS is an X-linked recessive form of pseudohermaphroditism due end-organ resistance to androgen. Affected males have female external genitalia, female breast development, blind vagina, absent uterus and female adnexa, and abdominal or inguinal testes, despite a normal 46,XY karyotype. Ref.4 Ref.16 Ref.18 Ref.52 Ref.66 Ref.68 Ref.71 Ref.73 Ref.74 Ref.75 Ref.76 Ref.77 Ref.78 Ref.80 Ref.81 Ref.85 Ref.86 Ref.88 Ref.90 Ref.92 Ref.94 Ref.96 Ref.105 Ref.106 Ref.107 Ref.109 Ref.110 Ref.111 Ref.112 Ref.113 Ref.114 Ref.116 Ref.117 Ref.119 Ref.120 Ref.121 Ref.127 Ref.129 Ref.130 Ref.133 Ref.134 Ref.136 Ref.137 Ref.138 Ref.139 Ref.142 Ref.145 Ref.146 Ref.147 Ref.150 Ref.152 Ref.153 Ref.154 Ref.155 Ref.156 Ref.157 Ref.158 Ref.159 Ref.160 Ref.162 Ref.165 Ref.166 Ref.171 Ref.172 Ref.173 Ref.174 Ref.178 Ref.181 Ref.182 Ref.185 Ref.186 Ref.188 Ref.191Defects in AR are the cause of spinal and bulbar muscular atrophy X-linked type 1 (SMAX1) [

MIM:313200]; also known as Kennedy disease. SMAX1 is an X-linked recessive form of spinal muscular atrophy. Spinal muscular atrophy refers to a group of neuromuscular disorders characterized by degeneration of the anterior horn cells of the spinal cord, leading to symmetrical muscle weakness and atrophy. SMAX1 occurs only in men. Age at onset is usually in the third to fifth decade of life, but earlier involvement has been reported. It is characterized by slowly progressive limb and bulbar muscle weakness with fasciculations, muscle atrophy, and gynecomastia. The disorder is clinically similar to classic forms of autosomal spinal muscular atrophy. Note=Caused by trinucleotide CAG repeat expansion. In SMAX1 patients the number of Gln ranges from 38 to 62. Longer expansions result in earlier onset and more severe clinical manifestations of the disease. Ref.190Note=Defects in AR may play a role in metastatic prostate cancer. The mutated receptor stimulates prostate growth and metastases development despite of androgen ablation. This treatment can reduce primary and metastatic lesions probably by inducing apoptosis of tumor cells when they express the wild-type receptor.Defects in AR are the cause of androgen insensitivity syndrome partial (PAIS) [

MIM:312300]; also known as Reifenstein syndrome. PAIS is characterized by hypospadias, hypogonadism, gynecomastia, genital ambiguity, normal XY karyotype, and a pedigree pattern consistent with X-linked recessive inheritance. Some patients present azoospermia or severe oligospermia without other clinical manifestations.

Miscellaneous: In the absence of ligand, steroid hormone receptors are thought to be weakly associated with nuclear components; hormone binding greatly increases receptor affinity. The hormone-receptor complex appears to recognize discrete DNA sequences upstream of transcriptional start sites.Transcriptional activity is enhanced by binding to RANBP9.The level of tyrosine phosphorylation may serve as a diagnostic tool to predict patient outcome in response to hormone-ablation therapy. Inhibition of tyrosine phosphorylation may be an effective intervention target for hormone-refractory prostate cancer.

Sequence similarities: Belongs to the nuclear hormone receptor family. NR3 subfamily.Contains 1 nuclear receptor DNA-binding domain.
Product References and Citations for anti-AR antibody
Yasumasa Ikeda, et al (2005), Androgen Receptor Gene Knockout Male Mice Exhibit Impaired Cardiac Growth and Exacerbation of Angiotensin II-induced Cardiac Fibrosis. J. Biol. Chem., Vol. 280, Issue 33, 29661-29666.

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