| http://purl.uniprot.org/citations/23399561 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23399561 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23399561 | http://www.w3.org/2000/01/rdf-schema#comment | "Upon starvation, cells undergo autophagy, an intracellular bulk-degradation process, to provide the required nutrients. Here, we observed that phospholipase C-related catalytically inactive protein (PRIP) binds to microtubule-associated protein 1 light chain 3 (LC3), a mammalian autophagy-related initiator that regulates the autophagy pathway. Then, we examined the involvement of PRIP in the nutrient depletion-induced autophagy pathway. Enhanced colocalization of PRIP with LC3 was clearly seen in nutrient-starved mouse embryonic fibroblasts under a fluorescent microscope, and interaction of the proteins was revealed by immunoprecipitation experiments with an anti-LC3 antibody. Under starvation conditions, there were more green fluorescent protein fused-LC3 dots in mouse embryonic fibroblasts from PRIP-deficient mice than in fibroblasts from wild type cells. The formation of new dots in a single cell increased, as assessed by time-lapse microscopy. Furthermore, the increase in autophagosome formation in PRIP-deficient cells was notably inhibited by exogenously overexpressed PRIP. Taken together, PRIP is a novel LC3-binding protein that acts as a negative modulator of autophagosome formation."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2013.01.119"xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2013.01.119"xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Harada K."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Harada K."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Hirata M."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Hirata M."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Matsuda M."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Matsuda M."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Takeuchi H."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Takeuchi H."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Tanida I."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Tanida I."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Mizokami A."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Mizokami A."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Kanematsu T."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Kanematsu T."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Umebayashi H."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/author | "Umebayashi H."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/name | "Biochem. Biophys. Res. Commun."xsd:string |
| http://purl.uniprot.org/citations/23399561 | http://purl.uniprot.org/core/name | "Biochem. Biophys. Res. Commun."xsd:string |