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with four transmembrane domains, such as truncated gonadotropin-releasing hormone receptor and V2 vasopressin receptor (No2), could act as an inhibitor to control the signaling of GPCR by directing degradation of full-length receptor and diminishing its
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Introduction Gonadotropin-releasing hormone (GnRH) is a hypothalamic decapeptide hormone known to regulate reproductive functions in mammals by modulating the biosynthesis and release of gonadotropins, namely luteinizing hormone (LH) and follicle
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gonadotropin and recombinant follicle-stimulating hormone in a pre- and postovulatory mouse follicle culture model . Fertility and Sterility 93 1464 – 1476 . ( doi:10.1016/j.fertnstert.2009.01.136 ) Forsythe JA Jiang BH Iyer NV Agani F Leung SW
Department of Cell Biology, Physiology and Immunology, University of Córdoba, Cordoba, Spain
Hospital Universitario Reina Sofia (HURS), Cordoba, Spain
CIBER de la Fisiopatología de la Obesidad y Nutrición (CIBERobn), Madrid, Spain
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(10 nM) for 4 h and 24 h (experiment for the comparison between the two somatostatin gene-encoded peptides); (4) NST or SST alone (10 nM) or in combination with acylated-ghrelin (10 nM) or gonadotropin-releasing hormone (GnRH, 10 nM) for 4 h. In
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diseases of 7TM receptor trafficking. Gonadotropin-releasing hormone I (pGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2, GnRH-I) acts via G αq -coupled 7TM receptors to stimulate phospholipase C (PLC). The consequent mobilization of Ca 2+ and activation
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central processors in the regulation of gonadotropin-releasing hormone secretion. Endocrinology 147 1154 –1158. Flier JS 2006 AgRP in energy balance: will the real AgRP please stand up? Cell Metabolism 3 83 –85
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Helen Wills Neuroscience Institute, UC Berkeley, Berkeley, California, USA
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PCOS is an increased secretion of gonadotropin-releasing hormone (GnRH) causing changes in ovarian function via pituitary gonadotropins ( Chang 2007 , Goodarzi et al . 2011 ). RFRP-3 inhibits gonadotropin release via its action on hypothalamic GnRH
Max Planck Institute for Experimental Endocrinology, Department of Cell and Molecular Biology, Fritz-Lipmann-Institut, Institute of Biomedicine, Institute for Biochemistry, University of East Anglia, Feodor-Lynen-Str. 7, D-30625 Hannover, Germany
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Max Planck Institute for Experimental Endocrinology, Department of Cell and Molecular Biology, Fritz-Lipmann-Institut, Institute of Biomedicine, Institute for Biochemistry, University of East Anglia, Feodor-Lynen-Str. 7, D-30625 Hannover, Germany
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indicated that A5 not only enhances gonadotropin secretion following stimulation by gonadotrophin-releasing hormone (GnRH; Kawaminami et al . 2002 ), but also stimulates basal PRL secretion while counteracting thyrotrophin-releasing hormone (TRH) induced
Graham Centre for Agricultural Innovation, Wagga Wagga, New South Wales, Australia
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Graham Centre for Agricultural Innovation, Wagga Wagga, New South Wales, Australia
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School of Animal & Veterinary Sciences, Charles Sturt University, Wagga Wagga, New South Wales, Australia
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gonadotropin releasing hormone surge in the ewe . Endocrinology 139 1752 – 1760 . ( https://doi.org/10.1210/endo.139.4.5904 ) 10.1210/endo.139.4.5904 9528959 Caraty A Smith JT Lomet D Ben Saïd S Morrissey A Cognie J Doughton B Baril G Briant C Clarke IJ
Animal Reproduction Laboratory, Department of Animal Science, Division of Animal Sciences, Texas A&M AgriLife Research Station, 3507 Highway 59E, Beeville, Texas 78102, USA
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Animal Reproduction Laboratory, Department of Animal Science, Division of Animal Sciences, Texas A&M AgriLife Research Station, 3507 Highway 59E, Beeville, Texas 78102, USA
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Animal Reproduction Laboratory, Department of Animal Science, Division of Animal Sciences, Texas A&M AgriLife Research Station, 3507 Highway 59E, Beeville, Texas 78102, USA
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Animal Reproduction Laboratory, Department of Animal Science, Division of Animal Sciences, Texas A&M AgriLife Research Station, 3507 Highway 59E, Beeville, Texas 78102, USA
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Introduction The pubertal initiation of high-frequency, episodic secretion of gonadotropin-releasing hormone (GnRH) is largely dependent upon metabolic cues throughout prepubertal development. Growth restriction during the juvenile period has been