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.
FUNCTION:SwissProt: P10275 # The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Activated, but not phosphorylated, by HIPK3. SIZE:919 amino acids; 98989 Da SUBUNIT:Binds DNA as a homodimer. Part of a ternary complex containing AR, EFCAB6/DJBP and PARK7. Interacts with HIPK3 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, SPDEF, SRA1, TGFB1I1, ZNF318 and RREB1. 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 ZMIZ1/ZIMP10 and ZMIZ2/ZMIP7 which both enhance its transactivation activity. Interacts with SLC30A9 (By similarity). SUBCELLULAR LOCATION:Nucleus. DOMAIN:SwissProt: P10275 Composed of three domains: a modulating N-terminal domain, a DNA-binding domain and a C-terminal steroid-binding domain. 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. PTM: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. DISEASE:SwissProt: P10275 # 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. SIMILARITY:Belongs to the nuclear hormone receptor family. NR3 subfamily. & Contains 1 nuclear receptor DNA-binding domain. 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.
Product Usage Statements
Quality Assurance
Routinely evaluated by immunoblot.
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.
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.
FUNCTION:SwissProt: P10275 # The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Activated, but not phosphorylated, by HIPK3. SIZE:919 amino acids; 98989 Da SUBUNIT:Binds DNA as a homodimer. Part of a ternary complex containing AR, EFCAB6/DJBP and PARK7. Interacts with HIPK3 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, SPDEF, SRA1, TGFB1I1, ZNF318 and RREB1. 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 ZMIZ1/ZIMP10 and ZMIZ2/ZMIP7 which both enhance its transactivation activity. Interacts with SLC30A9 (By similarity). SUBCELLULAR LOCATION:Nucleus. DOMAIN:SwissProt: P10275 Composed of three domains: a modulating N-terminal domain, a DNA-binding domain and a C-terminal steroid-binding domain. 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. PTM: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. DISEASE:SwissProt: P10275 # 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. SIMILARITY:Belongs to the nuclear hormone receptor family. NR3 subfamily. & Contains 1 nuclear receptor DNA-binding domain. 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.
Product Usage Statements
Quality Assurance
Routinely evaluated by immunoblot.
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.
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