http://purl.uniprot.org/citations/30661757 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/30661757 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/30661757 | http://www.w3.org/2000/01/rdf-schema#comment | "Hypothalamic melanocortin neurons play a pivotal role in weight regulation. Here, we examined the contribution of Semaphorin 3 (SEMA3) signaling to the development of these circuits. In genetic studies, we found 40 rare variants in SEMA3A-G and their receptors (PLXNA1-4; NRP1-2) in 573 severely obese individuals; variants disrupted secretion and/or signaling through multiple molecular mechanisms. Rare variants in this set of genes were significantly enriched in 982 severely obese cases compared to 4,449 controls. In a zebrafish mutagenesis screen, deletion of 7 genes in this pathway led to increased somatic growth and/or adiposity demonstrating that disruption of Semaphorin 3 signaling perturbs energy homeostasis. In mice, deletion of the Neuropilin-2 receptor in Pro-opiomelanocortin neurons disrupted their projections from the arcuate to the paraventricular nucleus, reduced energy expenditure, and caused weight gain. Cumulatively, these studies demonstrate that SEMA3-mediated signaling drives the development of hypothalamic melanocortin circuits involved in energy homeostasis."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.cell.2018.12.009"xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Park S."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Park S."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "O'Rahilly S."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "O'Rahilly S."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Jones E.Y."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Jones E.Y."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Kong Y."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Kong Y."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Barroso I."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Barroso I."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Simerly R.B."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Simerly R.B."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Farooqi I.S."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Farooqi I.S."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Keogh J.M."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Keogh J.M."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Papadia S."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Papadia S."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Bochukova E.G."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Bochukova E.G."xsd:string |
http://purl.uniprot.org/citations/30661757 | http://purl.uniprot.org/core/author | "Bounds R."xsd:string |