| http://purl.uniprot.org/citations/14512439 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/14512439 | http://www.w3.org/2000/01/rdf-schema#comment | "The gonadotropin beta-subunit mRNAs are differentially regulated by androgens. Testosterone (T) suppresses LH-beta and increases FSH-beta. We aimed to determine whether androgens regulate LH-beta and FSH-beta transcription [as measured by changes in primary transcript (PT)] and to determine whether androgens act directly on FSH-beta or via the intrapituitary activin/follistatin (FS) system. In castrate + GnRH antagonist-treated rats, T increased FSH-beta PT between 3 and 48 h. In contrast, T suppressed LH-beta PT. The increases in FSH-beta mRNA and PT were associated with reduced FS mRNA. Activin betaB mRNA was modestly suppressed. The increase in FSH-beta PT after T was androgen specific. Both T and dihydrotestosterone (DHT) increased FSH-beta PT 2-fold and decreased both FS and betaB mRNA. Estradiol suppressed FSH-beta PT 3-fold and had no effect on FS or betaB mRNAs. LH-beta PT was suppressed by DHT. To determine whether T stimulation of FSH-beta PT reflected a decrease in pituitary FS, we gave androgen in the presence of exogenous FS in vitro. T and DHT increased FSH-beta PT 2-to 3-fold. FS alone decreased FSH-beta PT 40% but did not diminish the increase FSH-beta PT in response to T. T, DHT, and FS did not affect FS mRNA, betaB mRNA, or LH-beta PT. In conclusion, androgens acting directly on the pituitary increase FSH-beta and decrease LH-beta transcription. The increase in FSH-beta PT in response to T was androgen specific and occurs in the presence of excess FS, suggesting that T stimulates FSH-beta transcription independently of modulation of FS."xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.org/dc/terms/identifier | "doi:10.1210/en.2003-1047"xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/author | "Marshall J.C."xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/author | "Dalkin A.C."xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/author | "Haisenleder D.J."xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/author | "Aylor K.W."xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/author | "Burger L.L."xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/author | "Prendergast K.A."xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/name | "Endocrinology"xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/pages | "71-78"xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/title | "Regulation of luteinizing hormone-beta and follicle-stimulating hormone (FSH)-beta gene transcription by androgens: testosterone directly stimulates FSH-beta transcription independent from its role on follistatin gene expression."xsd:string |
| http://purl.uniprot.org/citations/14512439 | http://purl.uniprot.org/core/volume | "145"xsd:string |
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