WordNet
- a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
- male sex hormone that is produced in the testes and responsible for typical male sexual characteristics (同)androgenic_hormone
PrepTutorEJDIC
- =sense organ / 受信装置
- アンドロゲン(男性ホルモン)
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/12/09 19:04:43」(JST)
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| Androgen receptor | |||||||||||||
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Structure of the ligand binding domain of the androgen receptor (rainbow cartoon) complexed with testosterone (white sticks).[1] |
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| Identifiers | |||||||||||||
| Symbols | AR; AIS; DHTR; HUMARA; HYSP1; KD; NR3C4; SBMA; SMAX1; TFM | ||||||||||||
| External IDs | OMIM: 313700 MGI: 88064 HomoloGene: 28 IUPHAR: NR3C4 ChEMBL: 1871 GeneCards: AR Gene | ||||||||||||
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| RNA expression pattern | |||||||||||||
| More reference expression data | |||||||||||||
| Orthologs | |||||||||||||
| Species | Human | Mouse | |||||||||||
| Entrez | 367 | 11835 | |||||||||||
| Ensembl | ENSG00000169083 | ENSMUSG00000046532 | |||||||||||
| UniProt | P10275 | P19091 | |||||||||||
| RefSeq (mRNA) | NM_000044 | NM_013476 | |||||||||||
| RefSeq (protein) | NP_000035 | NP_038504 | |||||||||||
| Location (UCSC) | Chr X: 66.76 – 66.95 Mb |
Chr X: 98.15 – 98.32 Mb |
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| PubMed search | [1] | [2] | |||||||||||
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| Androgen_recep | |||||||||
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crystal structure of the human androgen receptor ligand binding domain bound with an androgen receptor nh2-terminal peptide, ar20-30, and r1881
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| Identifiers | |||||||||
| Symbol | Androgen_recep | ||||||||
| Pfam | PF02166 | ||||||||
| InterPro | IPR001103 | ||||||||
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Normal function of the androgen receptor. Testosterone (T) enters the cell and, if 5-alpha-reductase is present, is converted into dihydrotestone (DHT). Upon steroid binding, the androgen receptor (AR) undergoes a conformational change and releases heat-shock proteins (hsps). Phosphorylation (P) occurs before or after steroid binding. The AR translocates to the nucleus where dimerization, DNA binding, and the recruitment of coactivators occur. Target genes are transcribed (mRNA) and translated into proteins.[2][3][4][5]
The androgen receptor (AR), also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4), is a type of nuclear receptor[6] that is activated by binding of either of the androgenic hormones testosterone or dihydrotestosterone [7] in the cytoplasm and then translocating into the nucleus. The androgen receptor is most closely related to the progesterone receptor, and progestins in higher dosages can block the androgen receptor.[8][9]
The main function of the androgen receptor is as a DNA-binding transcription factor that regulates gene expression;[10] however, the androgen receptor has other functions as well.[11] Androgen regulated genes are critical for the development and maintenance of the male sexual phenotype.
Contents
- 1 Function
- 1.1 Effect on development
- 1.2 Mechanism of action
- 1.2.1 Genomic
- 1.2.2 Non-genomic
- 2 Genetics
- 2.1 Gene
- 2.2 AR deficiencies
- 3 Structure
- 3.1 Isoforms
- 3.2 Domains
- 4 Interactions
- 5 See also
- 6 References
- 7 External links
Function[edit]
Effect on development[edit]
In some cell types, testosterone interacts directly with androgen receptors, whereas, in others, testosterone is converted by 5-alpha-reductase to dihydrotestosterone, an even more potent agonist for androgen receptor activation.[12] Testosterone appears to be the primary androgen receptor-activating hormone in the Wolffian duct, whereas dihydrotestosterone is the main androgenic hormone in the urogenital sinus, urogenital tubercle, and hair follicles.[13] Hence, testosterone is responsible primarily for the development of male primary sexual characteristics, whereas dihydrotestosterone is responsible for secondary male characteristics.
Androgens cause slow epiphysis, or maturation of the bones, but more of the potent epiphysis effect comes from the estrogen produced by aromatization of androgens. Steroid users of teen age may find that their growth had been stunted by androgen and/or estrogen excess. People with too little sex hormones can be short during puberty but end up taller as adults as in androgen insensitivity syndrome or estrogen insensitivity syndrome.[14]
Also, AR knockout-mice studies have shown that AR is essential for normal female fertility, being required for development and full functionality of the ovarian follicles and ovulation, working through both intra-ovarian and neuroendocrine mechanisms.[15]
Mechanism of action[edit]
Genomic[edit]
The primary mechanism of action for androgen receptors is direct regulation of gene transcription. The binding of an androgen to the androgen receptor results in a conformational change in the receptor that, in turn, causes dissociation of heat shock proteins, transport from the cytosol into the cell nucleus, and dimerization. The androgen receptor dimer binds to a specific sequence of DNA known as a hormone response element. Androgen receptors interact with other proteins in the nucleus, resulting in up- or down-regulation of specific gene transcription.[16] Up-regulation or activation of transcription results in increased synthesis of messenger RNA, which, in turn, is translated by ribosomes to produce specific proteins. One of the known target genes of androgen receptor activation is insulin-like growth factor I (IGF-1).[17] Thus, changes in levels of specific proteins in cells is one way that androgen receptors control cell behavior.
One function of androgen receptor that is independent of direct binding to its target DNA sequence, is facilitated by recruitment via other DNA-binding proteins. One example is serum response factor, a protein that activates several genes that cause muscle growth.[18]
Androgen receptor is modified by acetylation, which directly promotes contact independent growth of prostate cancer cells.[19]
Non-genomic[edit]
More recently, androgen receptors have been shown to have a second mode of action. As has been also found for other steroid hormone receptors such as estrogen receptors, androgen receptors can have actions that are independent of their interactions with DNA.[11][20] Androgen receptors interact with certain signal transduction proteins in the cytoplasm. Androgen binding to cytoplasmic androgen receptors can cause rapid changes in cell function independent of changes in gene transcription, such as changes in ion transport. Regulation of signal transduction pathways by cytoplasmic androgen receptors can indirectly lead to changes in gene transcription, for example, by leading to phosphorylation of other transcription factors.
Genetics[edit]
Gene[edit]
In humans, the androgen receptor is encoded by the AR gene located on the X chromosome at Xq11-12.[21][22]
AR deficiencies[edit]
The androgen insensitivity syndrome, formerly known as testicular feminization, is caused by a mutation of the androgen receptor gene located on the X chromosome (locus:Xq11-Xq12).[23] The androgen receptor seems to affect neuron physiology and is defective in Kennedy's disease.[24][25] In addition, point mutations and trinucleotide repeat polymorphisms has been linked to a number of additional disorders.[26]
Structure[edit]
Structural domains of the two isoforms (AR-A and AR-B) of the human androgen receptor. Numbers above the bars refer to the amino acid residues that separate the domains starting from the N-terminus (left) to C-terminus (right). NTD = N-terminal domain, DBD = DNA binding domain. LBD = ligand binding domain. AF = activation function.
Isoforms[edit]
Two isoforms of the androgen receptor (A and B) have been identified:[27]
- AR-A - 87 kDa - N-terminus truncated (lacks the first 187 amino acids), which results from in vitro proteolysis.[28]
- AR-B - 110 kDa - full length
Domains[edit]
Like other nuclear receptors, the androgen receptor is modular in structure and is composed of the following functional domains labeled A through F:[29]
- A/B) - N-terminal regulatory domain contains:[30]
- activation function 1 (AF-1) between residues 101 and 370 required for full ligand activated transcriptional activity
- activation function 5 (AF-5) between residues 360-485 is responsible for the constitutive activity (activity without bound ligand)
- dimerization surface involving residues 1-36 (containing the FXXLF motif where F = phenylalanine, L = leucine, and X = any amino acid residue) and 370-494, both of which interact with the LBD in an intramolecular[31][32][33] head-to-tail interaction[34][35][36]
- C) - DNA binding domain (DBD)
- D) - Hinge region - flexible region that connects the DBD with the LBD; along with the DBD, contains a ligand dependent nuclear localization signal[37]
- E) - Ligand binding domain (LBD) containing
- activation function 2 (AF-2), responsible for agonist induced activity (activity in the presence of bound agonist)
- AF-2 binds either the N-terminal FXXFL motif intramolecularly or coactivator proteins (containing the LXXLL or preferably FXXFL motifs)[36]
- A ligand dependent nuclear export signal[38]
- F) - C-terminal domain
Interactions[edit]
Androgen receptor has been shown to interact with:
- AKT1,[39]
- BAG1,[40][41][42]
- Beta-catenin,[43][44][45][46][47][48]
- BRCA1,[49][50]
- C-jun,[51]
- Calmodulin 1,[52]
- Caveolin 1,[53]
- CDK9,[54]
- COX5B,[55]
- CREB-binding protein,[56][57][58][59]
- Cyclin D1,[60][61][62]
- Cyclin-dependent kinase 7,[63]
- Death associated protein 6,[64]
- Deleted in Colorectal Cancer,[65]
- EFCAB6,[66]
- Epidermal growth factor receptor,[67][68]
- FOXO1,[69]
- GAPDH,[70]
- Gelsolin,[71]
- GNB2L1,[72]
- GSK3B,[73]
- HDAC1,[74]
- HSP90AA1,[75][76]
- HTATIP,[74]
- MAGEA11,[77][78]
- MED1,[79]
- MYST2,[80]
- NCOA1,[44][81][82]
- NCOA2,[43][58][77][83][84]
- NCOA3,[83][85][86]
- NCOA4,[39][84][87][88][89][90][91][92][93]
- NCOA6,[94]
- NCOR2,[43][95][96]
- NONO,[58]
- PA2G4,[97]
- PAK6,[98][99]
- PATZ1,[100]
- PIAS2,[101][102]
- PRPF6,[103]
- PTEN,[104]
- RAD9A,[105]
- RANBP9,[106]
- RCHY1,[107]
- Retinoblastoma protein,[108][109]
- RNF14,[84][87][110][111]
- RNF4,[100][112][113]
- SART3,[114]
- SMAD3,[115][116][117]
- Small heterodimer partner,[118]
- Src,[104][119][120]
- SRY,[121]
- STAT3,[122][123]
- SVIL,[124]
- Testicular receptor 2,[125]
- Testicular receptor 4,[126]
- TGFB1I1,[87][127]
- TMF1,[128]
- TRIM68,[129]
- UBE2I,[43][44][130][131][132][133]
- UXT,[134] and
- ZMIZ1.[135]
See also[edit]
- Androgen
- Discovery and development of antiandrogens
References[edit]
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- ^ Quigley CA, De Bellis A, Marschke KB, el-Awady MK, Wilson EM, French FS (June 1995). "Androgen receptor defects: historical, clinical, and molecular perspectives". Endocr. Rev. 16 (3): 271–321. doi:10.1210/edrv-16-3-271. PMID 7671849.
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External links[edit]
- GeneReviews/NCBI/NIH/UW entry on Androgen Insensitivity Syndrome
- OMIM entries on Androgen Insensitivity Syndrome
- GeneReviews/NIH/NCBI/UW entry on Spinal and Bulbar Muscular Atrophy, Kennedy's Disease, SBMA, X-Linked Spinal and Bulbar Muscular Atrophy
- OMIM entries on Spinal and Bulbar Muscular Atrophy, Kennedy's Disease, SBMA, X-Linked Spinal and Bulbar Muscular Atrophy
- Androgen Receptors at the US National Library of Medicine Medical Subject Headings (MeSH)
- Brinkmann AO. "Androgen physiology: receptor and metabolic disorders". In Robert McLachlan, editor. Endocrinology of Male Reproduction. Endotext.org. Retrieved 2008-04-29.
- Gottlieb B (2007-07-24). "The Androgen Receptor Gene Mutations Database Server". McGill University. Archived from the original on 22 April 2008. Retrieved 2008-04-29.
- Thompson J (2006-09-30). "Molecular Mechanisms of Androgen Receptor Interactions". Helsinki University Biomedical Dissertations No. 80. University of Helsinki. Archived from the original on 6 April 2008. Retrieved 2008-04-29.
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UpToDate Contents
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- 1. アンドロゲン受容体障害の診断および治療 diagnosis and treatment of disorders of the androgen receptor
- 2. アンドロゲン受容体障害の臨床症状および病因 clinical manifestations and pathogenesis of disorders of the androgen receptor
- 3. 転移性前立腺癌に対するセカンドラインホルモン療法 second line hormone therapy for metastatic prostate cancer
- 4. 転移性乳癌の全身治療：内分泌療法 systemic treatment for metastatic breast cancer endocrine therapy
- 5. 去勢抵抗性転移性前立腺癌に対するアビラテロンおよび新規抗アンドロゲン剤 abiraterone and newer antiandrogen compounds for castrate resistant metastatic prostate cancer
English Journal
- Atorvastatin induces autophagy in prostate cancer PC3 cells through activation of LC3 transcription.
- Toepfer N, Childress C, Parikh A, Rukstalis D, Yang W.SourceGeisinger Clinic; Danville, PA USA.
- Cancer biology & therapy.Cancer Biol Ther.2011 Oct 15;12(8). [Epub ahead of print]
- Our previous studies have demonstrated that atorvastatin induces autophagy in the androgen receptor negative prostate cancer PC3 cells through inhibition of geranylgeranyl biosynthesis [Parikh et al., Prostate. 70(9): 971-981 (2010)]. This study attempts to elucidate the molecular mechanism underlyi
- PMID 21768780
- Inability of NCoR/SMRT to repress androgen receptor transcriptional activity in prostate cancer cell lines.
- Laschak M, Bechtel M, Spindler KD, Hessenauer A.SourceInstitute of General Zoology and Endocrinology, Ulm University, Albert-Einstein-Allee 11, D-89069 Ulm, Germany.
- International journal of molecular medicine.Int J Mol Med.2011 Oct;28(4):645-51. doi: 10.3892/ijmm.2011.735. Epub 2011 Jun 27.
- The molecular mechanisms leading to castration-resistant prostate cancer (CRPC) are poorly understood. Among several mechanisms leading to CRPC growth a dysregulation of androgen receptor (AR) co-regulators (i.e. up-regulation of co-activators or down-regulation of co-repressors) is discussed. There
- PMID 21720703
Japanese Journal
- Epigenetic setting for long-term expression of estrogen receptor α and androgen receptor in cells.
- Imamura Takuya
- Hormones and behavior 59(3), 345-352, 2011-03
- … Epigenetic regulation of the nuclear estrogen and androgen receptors, ER and AR, constitutes the molecular basis for the long-lasting effects of sex steroids on gene expression in cells. … The effects prevail at hundreds of gene loci in the proximity of estrogen- and androgen-responsive elements and many more such loci through intra- and even inter-chromosomal level regulation. … The factors affecting the DNA methylation of the ERα and AR genes in cells include estrogen and androgen. …
- NAID 120002970855
- アンドロゲン受容体の標的ネットワークの同定--ゲノム医学的手法による系統的なアンドロゲン受容体下流因子の同定 (第1土曜特集 エネルギー代謝転写因子ネットワークと生活習慣病) -- (転写因子ネットワークシステムの新しい俯瞰)
- 高山 賢一,井上 聡
- 医学のあゆみ 237(6), 646-652, 2011-05-07
- NAID 40018778620
Related Links
- The androgen receptor (AR), also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4), is a type of nuclear receptor that is activated by binding of either of the androgenic hormones testosterone or dihydrotestosterone in ...
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| リンク元 | 「アンドロゲン受容体」「男性ホルモン受容体」 |