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http://purl.uniprot.org/citations/23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23321696http://www.w3.org/2000/01/rdf-schema#comment"The decapeptide GnRH is an important regulator of reproductive behavior and function. In the extracellular matrix, GnRH is metabolized by the endopeptidase EC3.4.24.15 (EP24.15) to generate the pentapeptide GnRH-(1-5). In addition to its expression in the adult hypothalamus, EP24.15 is expressed along the migratory path of GnRH-expressing neurons during development. Although we have previously demonstrated a role for EP24.15 in the generation of the biologically active pentapeptide GnRH-(1-5) in regulating GnRH expression and mediating sexual behavior during adulthood in rodents, the modulatory role of GnRH-(1-5) in the migration of GnRH neurons during development remains unknown. To address this information gap, we examined the effect of GnRH-(1-5) on the cellular migration of a premigratory GnRH-secreting neuronal cell line, the GN11 cell, using a wound-healing assay. Dose- and time-response studies demonstrated that GnRH-(1-5) significantly delayed wound closure. We then sought to identify the mechanism by which GnRH-(1-5) inhibits migration. Because the cognate GnRH receptor is a G protein-coupled receptor, we examined whether GnRH-(1-5) regulates migration by also activating a G protein-coupled receptor. Using a high-throughput β-arrestin recruitment assay, we identified an orphan G protein-coupled receptor (GPR173) that was specifically activated by GnRH-(1-5). Interestingly, small interfering RNA to GPR173 reversed the GnRH-(1-5)-mediated inhibition on migration of GN11 neurons. Furthermore, we also demonstrate that the GnRH-(1-5)-activated GPR173-dependent signal transduction pathway involves the activation of the signal transducer and activator of transcription 3 in GnRH migration. These findings indicate a potential regulatory role for GnRH-(1-5) in GnRH neuronal migration during development."xsd:string
http://purl.uniprot.org/citations/23321696http://purl.org/dc/terms/identifier"doi:10.1210/en.2012-1746"xsd:string
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/author"Mani S.K."xsd:string
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/author"Larco D.O."xsd:string
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/author"Wu T.J."xsd:string
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/author"Cho-Clark M."xsd:string
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/name"Endocrinology"xsd:string
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/pages"783-795"xsd:string
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/title"The metabolite GnRH-(1-5) inhibits the migration of immortalized GnRH neurons."xsd:string
http://purl.uniprot.org/citations/23321696http://purl.uniprot.org/core/volume"154"xsd:string
http://purl.uniprot.org/citations/23321696http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23321696
http://purl.uniprot.org/citations/23321696http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23321696
http://purl.uniprot.org/uniprot/Q6PI62#attribution-07C0874451016E792A000060FF44A382http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/P13562#attribution-476B9DEE3374574BA98E535E1BE559B6http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/P42227#attribution-D4F8909A3F8B21CC9B9F4A868DD14B9Fhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/#_A0A286YDB0-mappedCitation-23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/#_B7ZC18-mappedCitation-23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/#_Q14AC4-mappedCitation-23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/#_Q3ULI4-mappedCitation-23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/#_Q3UTE9-mappedCitation-23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/#_Q3U6S9-mappedCitation-23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/#_P13562-mappedCitation-23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23321696
http://purl.uniprot.org/uniprot/#_P42227-mappedCitation-23321696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23321696