| http://purl.uniprot.org/citations/19619494 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19619494 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19619494 | http://www.w3.org/2000/01/rdf-schema#comment | "Mitochondria are essential organelles that produce most of the energy for a cell, but concomitantly accumulate oxidative damage. Degradation of damaged mitochondria is critical for cell homeostasis, and this process is thought to be mediated by mitophagy, an autophagy-related pathway specific for mitochondria. However, whether mitochondria are selectively degraded, and how the autophagic machinery is targeted to mitochondria, remain largely unknown. Here we demonstrate that, in post-log phase cells under respiratory conditions, a substantial fraction of mitochondria are exclusively sequestered as cargoes and transported to the vacuole, a lytic compartment in yeast, in an autophagy-dependent manner. Interestingly, we found Atg32, a mitochondria-anchored protein essential for mitophagy that is induced during respiratory growth. In addition, our data suggest that Atg32 interacts with Atg8 and Atg11, autophagy-related proteins critical for recognition of cargo receptors. We propose that Atg32 acts as a mitophagy-specific receptor and regulates selective degradation of mitochondria."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.devcel.2009.06.013"xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.devcel.2009.06.013"xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/author | "Okamoto K."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/author | "Okamoto K."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/author | "Ohsumi Y."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/author | "Ohsumi Y."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/author | "Kondo-Okamoto N."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/author | "Kondo-Okamoto N."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/name | "Dev. Cell"xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/name | "Dev. Cell"xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/pages | "87-97"xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/pages | "87-97"xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/title | "Mitochondria-anchored receptor Atg32 mediates degradation of mitochondria via selective autophagy."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/title | "Mitochondria-anchored receptor Atg32 mediates degradation of mitochondria via selective autophagy."xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/volume | "17"xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://purl.uniprot.org/core/volume | "17"xsd:string |
| http://purl.uniprot.org/citations/19619494 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19619494 |
| http://purl.uniprot.org/citations/19619494 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19619494 |
| http://purl.uniprot.org/citations/19619494 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19619494 |
| http://purl.uniprot.org/citations/19619494 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19619494 |