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http://purl.uniprot.org/citations/24746696http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24746696http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24746696http://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/24746696http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2014.02.034"xsd:string
http://purl.uniprot.org/citations/24746696http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2014.02.034"xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Chen L."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Chen L."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Cai X."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Cai X."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Chen Q."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Chen Q."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Chen G."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Chen G."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Feng D."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Feng D."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Huang L."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Huang L."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Liu L."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Liu L."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Shen Y."xsd:string
http://purl.uniprot.org/citations/24746696http://purl.uniprot.org/core/author"Shen Y."xsd:string