The GPR54 gene as a regulator of puberty.
By S. Seminara, S. Messager, E. Chatzidaki, R. Thresher, J. Acierno, Jenna K Shagoury, Y. Bo-Abbas, W. Kuohung, K. M. Schwinof, Alan G Hendrick and 10 more. New England Journal of Medicine, 2004
1,326 citations recorded by the source corpus.
Subfields: Molecular Biology, Reproductive Medicine
View Paper: https://www.semanticscholar.org/paper/041e43adab59822ffb884d01234bc8fec232741a
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Citations in the corpus
- Biosocial Development and Delinquent Involvement (2005, background): “Recent research, for example, has identified the GPR54 gene as the gene responsible for the onset of pubertal development (Seminara et al., 2003).”
- 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).”
- Kisspeptins and reproduction: physiological roles and regulatory mechanisms. (2012, background): “Such seminal findings in humans were reinforced by the simultaneous report that mice engineered to lack functional Gpr54 were a complete phenocopy of affected patients (132, 401), a condition that was later confirmed in Kiss1 null mice (93, 234), even though Kiss1 KO animals appear to have a milder ”
- Neuroendocrinology of reproduction in teleost fish. (2010, background): “The role of GPR54 in eliciting this phenotype was further confirmed by knockout studies in mice (Seminara et al., 2003).”
- Kisspeptin neurons in the arcuate nucleus of the ewe express both dynorphin A and neurokinin B. (2007, background): “5756 Endocrinology, December 2007, 148(12):5752–5760 Goodman et al.”
- Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males. (2005, background): “GPR54-deficient (GPR54 / ) mice have abnormal sexual development, have low circulating gonadotropin concentrations, and are infertile (5, 6).”
- 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).”
- TAC3 and TACR3 Mutations in Familial Hypogonadotropic Hypogonadism Reveal a Key Role for Neurokinin B in the Central Control of Reproduction (2008, positive): “Recently, through a combination of human and mouse genetics, the hypothalamically expressed peptide kisspeptin and its receptor GPR54 have been established to be necessary for normal GnRH secretion and thus gonadotrope functio”