ABSTRACT
Although the functions of kisspeptin originally were believed to be restricted to
metastasis suppression, a novel role for this protein was discovered in 2003. Loss-of-function
mutations in its receptor, GPR54 , were found to cause absence of puberty and hypogonadotropic hypogonadism in humans.
Mice with targeted deletions of Gpr54 also have a hypogonadotropic phenotype, confirming the important role of this ligand-receptor
family in the control of puberty and reproductive function. Since these discoveries,
the peptide products of the KISS1 gene have been shown to be powerful stimulators of the gonadotropic axis. This review
examines the role of kisspeptins and GPR54 in reproductive function.
KEYWORDS
Kisspeptin - Metastin -
GPR54
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Stephanie B SeminaraM.D.
Reproductive Endocrine Unit, BHX 5, Massachusetts General Hospital
Fruit Street, Boston MA 02114
Email: seminara.stephanie@mgh.harvard.edu