Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 21, Issue 9, Pages 562-568Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2010.05.006
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Funding
- NICHD/NIH [U54 HD012303]
- NIH [R03 HD054595, R21 HD058752, R01 HD057549, R01 HD020377, R01 DK044838, K01 DK080467]
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD057549, P50HD012303, T32HD007203, U54HD012303] Funding Source: NIH RePORTER
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD020377, R21HD058752, R03HD054595] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K01DK080467, R01DK044838] Funding Source: NIH RePORTER
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Follicle-stimulating hormone (FSH), produced by pituitary gonadotrope cells, is required for maturation of ovarian follicles. The FSH beta subunit is the limiting factor for production of mature hormone and provides biological specificity. Activin dramatically induces FSH beta transcription and the secondary rise in FSH, important for follicular development, is dependent on this induction. Thus, regulation of FSH beta levels by activin is crucial for female reproductive fitness. This review discusses activin signaling pathways, transcription factors and FSH beta promoter elements required for activin responsiveness. Because FoxL2, a forkhead transcription factor, was recently shown to be instrumental in relaying activin signaling to the FSH beta promoter, we focus in this paper on its role and the inter-relatedness of several key players in activin responsiveness on the FSH beta promoter.
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