Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54
By N. de Roux, Emmanuelle Génin, J. Carel, F. Matsuda, J. Chaussain, E. Milgrom. Proceedings of the National Academy of Sciences of the United States of America, 2003
2,310 citations recorded by the source corpus.
Subfields: Endocrine and Autonomic Systems, Reproductive Medicine
View Paper: https://www.semanticscholar.org/paper/207e711ff248ff33066e02bfd5542b302afb821d
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In Endocrine and Autonomic Systems
In Reproductive Medicine
Citations in the corpus
- Kisspeptin signaling in the brain. (2009, background): “Various disabling mutations in KISS1R have been shown to occur in humans (23), and these mutations have involved deletion of as many as 155 nucleotides or as few as a single-nucleotide variant (L148S) in the second intracellular loop of the KISS1R gene (7, 24, 25).”
- Developmental and hormonally regulated messenger ribonucleic acid expression of KiSS-1 and its putative receptor, GPR54, in rat hypothalamus and potent luteinizing hormone-releasing activity of KiSS-1 peptide. (2004, background): “In this context, the demonstration that inactivating mutations of their putative receptor led to reproductive failure due to hypogonadotropic hypogonadism highlighted a previously unsuspected role for the KiSS-1/ GPR54 system in the control of the gonadotropic axis (8, 9).”
- Postnatal development of kisspeptin neurons in mouse hypothalamus; sexual dimorphism and projections to gonadotropin-releasing hormone (GnRH) neurons (2006, background): “Studies in humans and mice have demonstrated the absolute necessity of GPR54 for puberty onset (7, 8), and administration of kisspeptin to juvenile rodents and primates activates gonadotropin secretion (9–11).”
- Kisspeptins and reproduction: physiological roles and regulatory mechanisms. (2012, background): “in patients with hypogonadotropic hypogonadism (95).”
- Kisspeptin neurons in the arcuate nucleus of the ewe express both dynorphin A and neurokinin B. (2007, background): “Mutations of GPR54 prevent the onset of puberty in humans (11, 12) and mice (13).”
- Neuroendocrinology of reproduction in teleost fish. (2010, background): “Pionneering studies (de Roux et al., 2003; Seminara et al., 2003) revealed that inactivating mutations in the G-coupled protein receptor 54 (GPR54, KiSS1r) resulted in idiopathic hypogonadotrophic hypogonadism, where the affected individuals did not undergo puberty.”
- Mammalian G proteins and their cell type specific functions. (2005, background): “Kisspeptins for example, a family of peptides derived from the metastasis suppressor gene Kiss-1, were shown to enhance hypothalamic gonadotropin-releasing hormone secretion via the GPR54 receptor (137, 220, 472), and genetic inactivation of GPR54 in mice or mutation in humans causes hypogonadotropi”
- Differential regulation of KiSS-1 mRNA expression by sex steroids in the brain of the male mouse. (2005, background): “• Testosterone Regulates KiSS-1 mRNA in the Male Mouse Endocrinology, July 2005, 146(7):2976–2984 2977”
- Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males. (2005, background): “GPR54 mutations have been shown to cause hypogonadotrophic hypogonadism in humans (5, 7, 8).”