| http://purl.uniprot.org/citations/15322553 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15322553 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15322553 | http://www.w3.org/2000/01/rdf-schema#comment | "Vascular proliferative disorders, such as atherosclerosis and restenosis, are the most common causes of severe cardiovascular diseases, but a common molecular mechanism remains elusive. Here, we identify and characterize a novel hyperplasia suppressor gene, named HSG (later re-named rat mitofusin-2). HSG expression was markedly reduced in hyper-proliferative vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rat arteries, balloon-injured Wistar Kyoto rat arteries, or ApoE-knockout mouse atherosclerotic arteries. Overexpression of HSG overtly suppressed serum-evoked VSMC proliferation in culture, and blocked balloon injury induced neointimal VSMC proliferation and restenosis in rat carotid arteries. The HSG anti-proliferative effect was mediated by inhibition of ERK/MAPK signalling and subsequent cell-cycle arrest. Deletion of the p21(ras) signature motif, but not the mitochondrial targeting domain, abolished HSG-induced growth arrest, indicating that rHSG-induced anti-proliferation was independent of mitochondrial fusion. Thus, rHSG functions as a cell proliferation suppressor, whereas dysregulation of rHSG results in proliferative disorders."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.org/dc/terms/identifier | "doi:10.1038/ncb1161"xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.org/dc/terms/identifier | "doi:10.1038/ncb1161"xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Guo X."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Guo X."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Guo Y."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Guo Y."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Li P."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Li P."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Li Q."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Li Q."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Ma D."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Ma D."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Yang D."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Yang D."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Tang J."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Tang J."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Qiu X."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Qiu X."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Wen S."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Wen S."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Chen K.-H."xsd:string |
| http://purl.uniprot.org/citations/15322553 | http://purl.uniprot.org/core/author | "Chen K.-H."xsd:string |