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Literature summary for 1.3.99.5 extracted from

  • Thomas, L.N.; Douglas, R.C.; Rittmaster, R.S.; Too, C.K.L.
    Overexpression of 5alpha-reductase type1 increases sensitivity of prostate cancer cells to low concentrations of testosterone (2009), Prostate, 69, 595-602.
    View publication on PubMed

Cloned(Commentary)

Cloned (Comment) Organism
transient expression of pTRE-5alphaR1 in LNGK-9 PCa cells. Addition of testosterone increases growth of pTRE-5alphaR1 transfectants by 54.1% over cells grown in the absence of testosterone, compared to 25.0% in control cells. Testosterone also increases secretion of prostate-specific antigen 17fold in the 5alphaR1-transfected cells Homo sapiens

Inhibitors

Inhibitors Comment Organism Structure
dutasteride inhibits 5alphaR1 and 5alphaR2; inhibits 5alphaR1 and 5alphaR2 Homo sapiens
additional information no inhibition of 5alphaR1 by tetracycline Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P18405 gene SRD5A1
-
Homo sapiens P31213 gene SRD5A2
-

Source Tissue

Source Tissue Comment Organism Textmining
LNGK-9 PCa cell
-
Homo sapiens
-

Synonyms

Synonyms Comment Organism
5alpha-reductase type1
-
Homo sapiens
5alpha-reductase type2
-
Homo sapiens
5alphaR1
-
Homo sapiens
5alphaR2
-
Homo sapiens

pH Optimum

pH Optimum Minimum pH Optimum Maximum Comment Organism
7.2
-
assay at Homo sapiens

General Information

General Information Comment Organism
additional information prostate cancer development is accompanied by a decrease in 5alphaR2 and an increase in 5alphaR1 Homo sapiens
physiological function conversion of testosterone to 5alpha-dihydrotestosterone by the enzymes 5alpha-reductase types 1, 5alphaR1, and 2, 5alphaR2, is important for normal and pathological growth of the prostate Homo sapiens
physiological function conversion of testosterone to 5alpha-dihydrotestosterone by the enzymes 5alpha-reductase types 1, 5alphaR1, and 2, 5alphaR2, is important for normal and pathological growth of the prostate. Upregulation of 5alphaR1 enhances the cellular response to low, but not high, concentrations of testosterone. This explains one mechanism by which castration-recurrent prostate cancer can proliferate in the presence of castrate levels of circulating testosterone Homo sapiens