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.

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