| http://purl.uniprot.org/citations/36815579 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/36815579 | http://www.w3.org/2000/01/rdf-schema#comment | "NG2-glia comprise a heterogeneous population of cycling cells that give rise to mature, myelinating oligodendrocytes. The mechanisms that regulate the process of differentiation from NG2-glia into oligodendrocytes are still not fully understood but over the last years the G Protein-coupled Receptor 17 (GPR17) has been on the spotlight as a possible key regulator. Interestingly, GPR17-expressing NG2-glia show under physiological conditions a slower and lower level of differentiation compared to NG2-glia without GPR17. In contrast, after a CNS insult these react with proliferation and differentiation in a high rate, pointing towards a role in repair processes. However, the role of GPR17+ NG2-glia under healthy conditions in adulthood has not been addressed yet. Therefore, we aimed here to characterize the GPR17-expressing NG2-glia. Using transgenic mouse models, we showed restricted GPR17 expression in only some NG2-glia. Furthermore, we found that these cells constitute a distinct subset within the NG2-glia population, which shows a different gene expression profile and behavior when compared to the total NG2-glia population. Genetic depletion of GPR17+ cells showed that these are not contributing to the dynamic and continuous generation of new oligodendrocytes in the adult brain. Taken together, GPR17+ NG2-glia seem to play a distinct role under physiological conditions that goes beyond their classic differentiation control, that needs to be further elucidated. These results open new avenues for using the GPR17 receptor as a target to change oligodendrogenesis under physiological and pathological conditions, highlighting the importance of further characterization of this protein for future pharmacological studies."xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.org/dc/terms/identifier | "doi:10.1002/glia.24356"xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/author | "Dimou L."xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/author | "Rossner M.J."xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/author | "Unger N."xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/author | "Kannaiyan N."xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/author | "Miralles A.J."xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/name | "Glia"xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/pages | "1536-1552"xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/title | "Analysis of the GPR17 receptor in NG2-glia under physiological conditions unravels a new subset of oligodendrocyte progenitor cells with distinct functions."xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://purl.uniprot.org/core/volume | "71"xsd:string |
| http://purl.uniprot.org/citations/36815579 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/36815579 |
| http://purl.uniprot.org/citations/36815579 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/36815579 |
| http://purl.uniprot.org/uniprot/#_Q6NS65-mappedCitation-36815579 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/36815579 |
| http://purl.uniprot.org/uniprot/Q6NS65 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/36815579 |