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07-1375 Anti-phospho-Androgen Receptor (Ser81) Antibody

Anti-phospho-Androgen Receptor (Ser81) Antibody is an antibody against phospho-Androgen Receptor (Ser81) for use in WB.

Anti-phospho-Androgen Receptor (Ser81) Antibody MSDS (material safety data sheet) or SDS, CoA and CoQ, dossiers, brochures and other available documents.
Research Category: Signaling, Epigenetics & Nuclear Function Research Sub-Category: Transcription Factors Gene Symbol: AR, androgen receptor, RP11-383C12.1, AIS, DHTR, HUMARA, KD, NR3C4, SBMA, SMAX1, TFM UniProt Number: P10275
07-1375
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Species ReactivityKey ApplicationsHostFormatAntibody Type
HWBRbAffinity PurifiedPolyclonal Antibody
Description
Catalogue Number07-1375
Brand Family Upstate
Trade Name
  • Upstate
DescriptionAnti-phospho-Androgen Receptor (Ser81) Antibody
Background InformationThe X-linked androgen receptor (Dihydrotestosterone receptor; Nuclear receptor subfamily 3 group C member 4) is a member of the family of NR3 ligand-dependent transcription factors characterized by a ligand binding domain at the C-terminus, a central DNA-binding domain, and N-terminal transcription- activation domains. Androgen receptors are activated by steroid hormones such as testosterone and dihydrotestosterone. Activated androgen receptors translocate from the cytoplasm to the nucleus where they form homodimers that bind DNA. The androgen receptor associates with a number of adaptor-like proteins and functions as a complex that may induce or repress transcription depending on whether its associated proteins are co-activators or co-repressors that affect transcription possibly by modifying chromatin; co-activators are involved in histone acetylation and transcriptional activation whereas co-repressors are involved in histone deactylation and transcriptional repression. The androgen receptor is important for determining sex and male characteristics. Defective androgen receptors may play a role in Reifenstein syndrome, Kennedy disease, as well as prostate cancer.
References
Product Information
FormatAffinity Purified
Control
  • R1881 (methyltrienolone) treated LNCap lysates
PresentationPurified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Quality LevelMQ100
Applications
ApplicationAnti-phospho-Androgen Receptor (Ser81) Antibody is an antibody against phospho-Androgen Receptor (Ser81) for use in WB.
Key Applications
  • Western Blotting
Biological Information
ImmunogenKLH-conjugated synthetic peptide corresponding to amino acids including and surrounding Ser81 of human Androgen Receptor.
HostRabbit
SpecificityDetects Androgen Receptor (AR) only when phosphorylated on Ser81
Species Reactivity
  • Human
Species Reactivity NotePrimate, Dog, Horse, and Cow expected based only 1 amino acid difference.
Antibody TypePolyclonal Antibody
Entrez Gene Number
Entrez Gene SummaryNP_000035.2
Gene Symbol
  • AR
  • androgen receptor
  • RP11-383C12.1
  • AIS
  • DHTR
  • HUMARA
  • KD
  • NR3C4
  • SBMA
  • SMAX1
  • TFM
Modifications
  • Phosphorylation
UniProt Number
UniProt SummaryFUNCTION: 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.
SIZE: 919 amino acids; 98989 Da
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.
SUBCELLULAR LOCATION: Nucleus
DOMAIN: Composed of three domains: a modulating N-terminal domain, a DNA-binding domain and a C-terminal steroid-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.
POST-TRANSLATIONAL MODIFICATIONS: Sumoylated on Lys-386 (major) and Lys-520. Phosphorylated 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.
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: Genetic variation in AR can be responsible of androgenetic alopecia (AGA) [MIM:109200].

Defects in AR are the cause of androgen insensibility syndrome (AIS) [MIM:300068]; previously known as testicular feminization syndrome (TFM). It can be complete (CAIS) when external genitalia are phenotypically female; or partial (PAIS) when external genitalia are substantively ambiguous or mild (MAIS) when external genitalia are normal male or nearly so.

Defects in AR are the cause of X-linked spinal and bulbar muscular atrophy (SBMA) [MIM:313200]; also known as Kennedy disease. In SBMA patients the number of Gln ranges from 40 to 52. Longer expansions result in earlier onset and more severe clinical manifestations of the disease.

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 may be the cause of infertility male syndrome [MIM:308370]; also called androgen insensitivity. It is characterized by azoospermia, elevated testosterone and luteinizing hormone plasma levels and an abnormal androgen receptor.

Defects in AR are the cause of Reifenstein syndrome [MIM:312300]; also known as partial androgen insensitivity. The features of this form of male pseudohermaphroditism are hypospadias, hypogonadism, gynecomastia, normal XY karyotype, and a pedigree pattern consistent with X-linked recessive inheritance.
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.
Molecular Weight110 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality AssuranceRoutinely evaluated by western blot on R1881 (methyltrienolone) treated LNCap lysates
Usage Statement
  • 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 and Shipping Information
Storage ConditionsStable for 1 year at 2-8°C from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
Packaging Information
Material Size200 µL
Transport Information
Supplemental Information
Specifications
Global Trade Item Number
Katalógusszám GTIN
07-1375 04053252677007

Documentation

Anti-phospho-Androgen Receptor (Ser81) Antibody MSDS

Title

Safety Data Sheet (SDS) 

Anti-phospho-Androgen Receptor (Ser81) Antibody Certificates of Analysis

TitleLot Number
Anti-phospho-Androgen Receptor (Ser81) - 2384004 2384004
Anti-phospho-Androgen Receptor (Ser81) - 2172777 2172777
Anti-phospho-Androgen Receptor (Ser81) - 2251782 2251782
Anti-phospho-Androgen Receptor (Ser81) - 2309344 2309344
Anti-phospho-Androgen Receptor (Ser81) - 2495664 2495664
Anti-phospho-Androgen Receptor (Ser81) - 3015824 3015824
Anti-phospho-Androgen Receptor (Ser81) - 3378753 3378753
Anti-phospho-Androgen Receptor (Ser81) - 4143306 4143306
Anti-phospho-Androgen Receptor (Ser81) - JBC1787300 JBC1787300
Anti-phospho-Androgen Receptor (Ser81) - NG1527856 NG1527856
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References

Reference overviewPub Med ID
Androgen receptor phosphorylation at serine 515 by Cdk1 predicts biochemical relapse in prostate cancer patients.
Willder, JM; Heng, SJ; McCall, P; Adams, CE; Tannahill, C; Fyffe, G; Seywright, M; Horgan, PG; Leung, HY; Underwood, MA; Edwards, J
British journal of cancer  108  139-48  2013

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