| http://purl.uniprot.org/citations/15607732 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15607732 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15607732 | http://www.w3.org/2000/01/rdf-schema#comment | "A lysophospholipid series, such as lysophosphatidic acid, lysophosphatidylserine, and lysophosphatidylcholine (LPC), is a bioactive lipid mediator with diverse physiological and pathological functions. LPC has been reported to induce insulin secretion from pancreatic beta-cells, however, the precise mechanism has remained elusive to date. Here we show that an orphan G-protein-coupled receptor GPR119 plays a pivotal role in this event. LPC potently enhances insulin secretion in response to high concentrations of glucose in the perfused rat pancreas via stimulation of adenylate cyclase, and dose-dependently induces intracellular cAMP accumulation and insulin secretion in a mouse pancreatic beta-cell line, NIT-1 cells. The Gs-protein-coupled receptor for LPC was identified as GPR119, which is predominantly expressed in the pancreas. GPR119-specific siRNA significantly blocked LPC-induced insulin secretion from NIT-1 cells. Our findings suggest that GPR119, which is a novel endogenous receptor for LPC, is involved in insulin secretion from beta-cells, and is a potential target for anti-diabetic drug development."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2004.11.120"xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2004.11.120"xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Matsumoto M."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Matsumoto M."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Ohishi T."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Ohishi T."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Saito T."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Saito T."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Ueda Y."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Ueda Y."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Yoshida S."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Yoshida S."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Matsumoto S."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Matsumoto S."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Soga T."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Soga T."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Matsui T."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Matsui T."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Momose K."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Momose K."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Matsushime H."xsd:string |
| http://purl.uniprot.org/citations/15607732 | http://purl.uniprot.org/core/author | "Matsushime H."xsd:string |