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PROK2-PROKR2 Signaling: New Contributor to Pleasant Touch.
Neurosci Bull
February 2023
School of Acupuncture and Tuina, Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Single-cell transcriptomics of suprachiasmatic nuclei reveal a Prokineticin-driven circadian network.
EMBO J
October 2021
Division of Neurobiology, MRC Laboratory of Molecular Biology, Cambridge, UK.
Circadian rhythms in mammals are governed by the hypothalamic suprachiasmatic nucleus (SCN), in which 20,000 clock cells are connected together into a powerful time-keeping network. In the absence of network-level cellular interactions, the SCN fails as a clock. The topology and specific roles of its distinct cell populations (nodes) that direct network functions are, however, not understood.
View Article and Find Full Text PDFThe PROK2/PROKR2 signaling pathway is required for the migration of most olfactory bulb interneurons.
J Comp Neurol
December 2019
State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, MOE Frontier Center for Brain Science, Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, PR China.
Neural stem cells in the subventricular zone (SVZ) of the lateral ventricle generate new interneurons, which migrate tangentially through the rostral migratory stream (RMS) to the olfactory bulb (OB). The PROK2 (prokineticin 2) and PROKR2 (prokineticin receptor 2) signaling pathway has been identified to cause human Kallmann syndrome, a developmental disease that associates hypogonadism with anosmia (OB developmental defects). However, the identities and properties of PROK2 and PROKR2 cells in the SVZ-RMS-OB remain largely unknown.
View Article and Find Full Text PDFThe mystery of puberty initiation: genetics and epigenetics of idiopathic central precocious puberty (ICPP).
J Endocrinol Invest
August 2017
Division of Endocrinology, Diabetes and Metabolism, First Department of Pediatrics, Faculty of Medicine, National and Kapodistrian University of Athens, Medical School, "Aghia Sofia" Children's Hospital, Athens, Greece.
Puberty is a major developmental stage. Damaging mutations, considered as "mistakes of nature", have contributed to the unraveling of the networks implicated in the normal initiation of puberty. Genes involved in the abnormal hypothalamic-pituitary-gonadal (HPG) axis development, in the normosmic idiopathic hypogonadotropic hypogonadism (nIHH), in the X-linked or autosomal forms of Kallmann syndrome and in precocious puberty have been identified (GNRH1, GNRHR, KISS1, GPR54, FGFR1, FGF8, PROK2, PROKR2, TAC3, TACR3, KAL1, PROK2, PROKR2, CHD7, LEP, LEPR, PC1, DAX1, SF-1, HESX-1, LHX3, PROP-1).
View Article and Find Full Text PDFPROK2/PROKR2 Signaling and Kallmann Syndrome.
Front Endocrinol (Lausanne)
April 2013
INSERM U1016, Institut Cochin, Université Paris-Descartes Paris, France.
Kallmann syndrome (KS) is a developmental disease that associates hypogonadism and a deficiency of the sense of smell. The reproductive phenotype of KS results from the primary interruption of the olfactory, vomeronasal, and terminal nerve fibers in the frontonasal region, which in turn disrupts the embryonic migration of neuroendocrine gonadotropin-releasing hormone (GnRH) synthesizing cells from the nose to the brain. This is a highly heterogeneous genetic disease, and mutations in any of the nine genes identified so far have been found in approximately 30% of the KS patients.
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