Status
Please wait ...

Details for receptor: AR

  • Top
  • General information
  • External resources
  • General information
  • Hormones
  • Anatomical structures
  • Click to access the toolbox
EndoNet ID: ENR00663

To link to the content of EndoNet use the EndoNet ID that is given on the detail pages in the format ENX0000, where X is a place holder for the type of the component (e. g. R for receptor or C for anatomical structure).
As URL for the linking append this ID to the detail page for this type of component.
For an hormone that would be: 

http://endonet.bioinf.med.uni-goettingen.de/hormone/ENH00000

It is also possible to use the search of EndoNet to link to the right detail page. The URL should look like 

http://endonet.bioinf.med.uni-goettingen.de/search/ENC00000
If the search pattern is unambigious the user is directed to the corresponding detail page.

Synonyms

  • androgen receptor
  • dihydrotestosterone receptor
  • DHT receptor
  • AR

General information

  • Activation reduces sperm motility and spermatozoa production. [1]
  • In the pre-antral follicle, AR was observed in the theca cells. [2]
  • Strong AR immunoreactivity was restricted to the nuclei of the apocrine secretory epithelium. [3]
  • The AR, ER-alpha and ER-beta are expressed in the growth plate and the osteoblasts. [4]
  • In granulosa and thecal cells of secondary follicles there was weak nuclear staining for AR. [5]
  • AR was detected in eccrine sweat glands, sebaceous glands and epidermis. [6]
  • AR is expressed in human adrenal cortex and the cancer cell line, NCI-H295. [7]

Links to other resources

UniProt P10275
Ensembl ENST00000396044

Binding hormones

  • DHT

Anatomical structures with this receptor

  • prostate

    Induced phenotypes

    • Androgen insensitivity syndromes
      • The androgen receptor (AR) is a high affinity receptor protein encoded on the human X-chromosome that mediates the actions of androgens during development and in the adult. Defects in this receptor protein result in a wide range of abnormalities of male sexual development. Studies in a number of different laboratories have identified mutations of the AR gene in subjects with androgen resistance syndromes. [8]

  • theca_cell

    Induced phenotypes

    • ovarian follicle development
      • Studies with AR knockout mice have revealed that AR function is essential for maintaining female fertility, notably through optimizing the conditions for follicular growth, final follicle development and ovulation. [9]
    • polycystic ovary syndrome
      • Hyperandrogenemia arises from ovarian or adrenal dysfunction or tumors, disturbed peripheral metabolism of androgen precursors or exogenous androgenic medications. [10]
      • Polycystic ovary syndrome, a polymorphic hyperandrogenic disorder, is often assiciated with insulin resistance and acanthosis nigricans in obese women, a combination termed Hair-An syndrome. [11]

  • granulosa_cell

    Induced phenotypes

    • ovarian follicle development
      • Studies with AR knockout mice have revealed that AR function is essential for maintaining female fertility, notably through optimizing the conditions for follicular growth, final follicle development and ovulation. [9]

  • eccrine_sweat_glands

    Induced phenotypes

    • positive regulation of perspiration
      • Androgens appear to promote perspiration since males sweat at a greater rate than females in similar situations. [12]

  • sebaceous_glands

    Induced phenotypes

    • sebaceous gland development
      • The development of the sebaceous gland depends on androgens. The administration of testosterone to castrated males, children or postmenopausal women in whom sebaceous secretion is normally low results in significant increase in sebaceous gland activity. Thus, the sebaqueous gland is an androgen target-organ. [13]

  • cell_of_apocrine_sweat_gland

  • growth_plate

    Induced phenotypes

    • regulation of pubertal skeletal growth
      • Androgen probably augments pubertal skeletal growth by growth factor produciton at the growth plate. [14]
    • positive regulation of bone mineralization
      • Testosterone appears to help maintain bone formation and serves as a substrate for aromatization to estrogen in peripheral tissues including bone. [14]

  • epidermis

    Induced phenotypes

    • negative regulation of epidermal barrier function
      • Androgens stimulates epidermal hyperplasia and suppresses epidermal barrier function in fetal and adult human skin. [15]
    • acne vulgaris
      • Several experimental observations, therapeutic experience as well as clinical observations support the pathogenic role of androgens in acne. In addition to stimulation of sebum production, indirect evidence also suggests the importance of androgens on comedogenesis and inflammation. [16]

  • osteoblast

    Influences

    • positive IGF-1
      • The nonaromatizable androgen, 5alpha-dihydrotestosterone (5alphaDHT), and testosterone, but not dehydroepiandrosterone, increased IGF-I messenger RNA (mRNA) levels up to 4-fold in a dose (10(-12)-10(-6) M)- and time (2-72 h)-dependent fashion. [17]
    • negative IGFBP-4
      • 5-alpha-DHT decreased IGFBP-4 mRNA and protein levels by 2- and 4-fold. [17]
    • positive IGFBP-2
      • 5-alpha-DHT increased IGFBP-2 and -3 mRNA and protein levels by 6- and 7-fold (for mRNA) and 3- and 5-fold (for protein). [17]
    • positive IGFBP-3
      • 5-alpha-DHT increased IGFBP-2 and -3 mRNA and protein levels by 6- and 7-fold (for mRNA) and 3- and 5-fold (for protein). [17]

  • hair_follicle

    Induced phenotypes

    • hair growth
      • Androgens have strong effects on hair growth and appear to act through the AR on dermal papilla cells. [18]
    • alopecia
      • Single nucleotide polymorohisms of the AR have been associated with androgenetic alopecia in men. [19]
    • hirsutism
      • Single nucleotide polymorphisms of the AR have been associated with hirsutism in women. [20]

  • adrenal_cortex

    Influences

    • positive TGF-beta 1
      • In a human adrenocortical cell line, DHT is capable of up-regulating both TGF-beta1 mRNA and protein. [7]

  • liver

    Induced phenotypes

    • mediation of effects from thymus on liver
      • The thymus plays an important role in maintaining the drug-metabolizing enzyme activity, anti-oxidative ability and biomembrane integrity in the liver of rats. These effects are mediated by sex hormones. Androgen mainly mediates the regulation of the thymus on liver drug-metabolizing enzymes in male rats. [21]

  • heart

    Induced phenotypes

    • cardiac hypertrophy
      • Androgen receptors are present in cardiac myocyte from multiple species and modulate the cardiac phenotype (hypertrophy), [22]
    • Isoform 2 is mainly expressed in heart and skeletal muscle. [23]

  • skeleton_muscle

    • Isoform 2 is mainly expressed in heart and skeletal muscle. [23]
Reference