http://purl.uniprot.org/citations/24746696 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/24746696 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/24746696 | http://www.w3.org/2000/01/rdf-schema#comment | "Mitochondrial autophagy, or mitophagy, is a major mechanism involved in mitochondrial quality control via selectively removing damaged or unwanted mitochondria. Interactions between LC3 and mitophagy receptors such as FUNDC1, which harbors an LC3-interacting region (LIR), are essential for this selective process. However, how mitochondrial stresses are sensed to activate receptor-mediated mitophagy remains poorly defined. Here, we identify that the mitochondrially localized PGAM5 phosphatase interacts with and dephosphorylates FUNDC1 at serine 13 (Ser-13) upon hypoxia or carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP) treatment. Dephosphorylation of FUNDC1 catalyzed by PGAM5 enhances its interaction with LC3, which is abrogated following knockdown of PGAM5 or the introduction of a cell-permeable unphosphorylated peptide encompassing the Ser-13 and LIR of FUNDC1. We further observed that CK2 phosphorylates FUNDC1 to reverse the effect of PGAM5 in mitophagy activation. Our results reveal a mechanistic signaling pathway linking mitochondria-damaging signals to the dephosphorylation of FUNDC1 by PGAM5, which ultimately induces mitophagy."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.molcel.2014.02.034"xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.molcel.2014.02.034"xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Chen L."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Chen L."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Cai X."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Cai X."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Chen Y."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Chen Y."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Chen Q."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Chen Q."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Chen G."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Chen G."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Feng D."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Feng D."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Huang L."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Huang L."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Liu X."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Liu X."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Liu L."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Liu L."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Shen Y."xsd:string |
http://purl.uniprot.org/citations/24746696 | http://purl.uniprot.org/core/author | "Shen Y."xsd:string |