The KiSS-1 receptor GPR54 is essential for the development of the murine reproductive system.

By S. Funes, J. Hedrick, G. Vassileva, L. Markowitz, S. Abbondanzo, A. Golovko, Shijun Yang, F. Monsma, E. Gustafson. Biochemical and Biophysical Research Communications - BBRC, 2003

668 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Reproductive Medicine

View Paper: https://www.semanticscholar.org/paper/e7c29f40f84d0446bf0b10432eb9819468751a99

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. S. Offermanns
2. N. Wettschureck

In Molecular Biology

1. D. Clifton
2. R. Steiner
3. S. Offermanns
4. N. Wettschureck

In Reproductive Medicine

1. D. Clifton
2. R. Steiner

Citations in the corpus

• Kisspeptin signaling in the brain. (2009, background): “Moreover, studies of mice bearing targeted deletions of Kiss1r produced the same phenotypic anomaly of reproductive dysfunction (8, 9).”
• 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”
• 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): “Similarly, GPR54 mRNA has been found in placenta, several areas of the central nervous system, pituitary, spinal cord, and pancreas (12, 14).”
• 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).”
• 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).”
• 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 ”