RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/31550518http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31550518http://www.w3.org/2000/01/rdf-schema#comment"The expression and functional impact of most orphan G-protein coupled receptors (GPCRs) in β-cell is not fully understood. Microarray expression indicated that 36 orphan GPCRs are restricted in human islets, while 55 receptors overlapped between human islets and INS-1 cells. GPR183 showed higher expression in diabetic compared to non-diabetic human islets. GPR183 expression co-localized with β-cells while it was lacking in α-cells in human islets. The GPR183 agonist (7α-25-DHC) potentiated insulin secretion and protected against glucotoxicity-induced β-cell damage in human islets. Silencing of GPR183 in INS-1 cells decreased the expression of proinsulin genes, Pdx1, Mafa and impaired insulin secretion with a concomitant decrease in cAMP generation. Cultured INS-1 cells with 7α-25-DHC were associated with increased proliferation and expression of GPR183, INS2, PDX1, NeuroD, and INSR. In conclusion, the beneficial impact of GPR183 activation on β-cell function makes it a potential therapeutic target to prevent or reverse β-cell dysfunction."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.org/dc/terms/identifier"doi:10.1016/j.mce.2019.110592"xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Hamad M."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Malek A."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Salehi A."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Mohammed I."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Duner P."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Taneera J."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Mohammed A.K."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Elemam N.M."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Sulaiman N."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Dhaiban S."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/author"Hachim M."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/name"Mol Cell Endocrinol"xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/pages"110592"xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/title"Orphan G-protein coupled receptor 183 (GPR183) potentiates insulin secretion and prevents glucotoxicity-induced beta-cell dysfunction."xsd:string
http://purl.uniprot.org/citations/31550518http://purl.uniprot.org/core/volume"499"xsd:string
http://purl.uniprot.org/citations/31550518http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31550518
http://purl.uniprot.org/citations/31550518http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31550518
http://purl.uniprot.org/uniprot/#_P32249-mappedCitation-31550518http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31550518
http://purl.uniprot.org/uniprot/P32249http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31550518