Cited by 606Autophagy in Disease and TherapyParkinson's Disease Mechanisms and TreatmentsUbiquitin and proteasome pathways

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PINK1/Parkin-mediated mitophagy in mammalian cells

Eiyama, Akinori, Okamoto, Koji·2015·Current Opinion in Cell Biology

DOI 10.1016/j.ceb.2015.01.002

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Abstract

Mitochondria-specific autophagy (mitophagy) is a fundamental process critical for maintaining mitochondrial fitness in a myriad of cell types. Particularly, mitophagy contributes to mitochondrial quality control by selectively eliminating dysfunctional mitochondria. In mammalian cells, the Ser/Thr kinase PINK1 and the E3 ubiquitin ligase Parkin act cooperatively in sensing mitochondrial functional state and marking damaged mitochondria for disposal via the autophagy pathway. Notably, ubiquitin and deubiquitinases play vital roles in modulating Parkin activity and mitophagy efficiency. In this review, we highlight recent breakthroughs addressing the key issues of how PINK1 activates Parkin in response to mitochondrial malfunction, how Parkin localizes specifically to impaired mitochondria, and how ubiquitination and deubiquitination regulate PINK1/Parkin-mediated mitophagy.

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Fiesel, 2014, A specific subset of E2 ubiquitin-conjugating enzymes regulate Parkin activation and mitophagy differently, J Cell Sci, 127, 3488

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Authors: Eiyama, A., & Okamoto, K.
Affiliations: The University of Osaka (JP)
Corresponding author: Okamoto, Koji
ORCID: Eiyama, Akinori
Okamoto, Koji
Venue: Current Opinion in Cell Biology
Publisher: Elsevier BV
Published: 2015-04
Volume: 33
Pages: 95-101
ISSN: 0955-0674 (ISSN-L)
DOI: 10.1016/j.ceb.2015.01.002
OpenAlex: W2013642338
Cited by: 603
References: 61
Citations by year: 2026: 45 · 2025: 66 · 2024: 71 · 2023: 74 · 2022: 83 · 2021: 68 · 2020: 57 · 2019: 36 · 2018: 38 · 2017: 22 · 2016: 29 · 2015: 14
FWCI: 4.42
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Current Opinion in Cell Biology (publishedVersion)
PubMed (publishedVersion)
Funders: Japan Society for the Promotion of Science (25291045, 25650067)
Ministry of Education, Culture, Sports, Science and Technology (26111513)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
Keywords: mitophagy, PINK1, Parkin, mitochondrial quality control, mitochondrial dysfunction, ubiquitination, deubiquitination, E3 ubiquitin ligase, Ser/Thr kinase, mammalian cells
MeSH terms: PTEN-Induced Putative Kinase, Animals, Enzyme Activation, Humans, Mammals, Mitochondria, Phosphorylation, Protein Kinases, Ubiquitin, Ubiquitin-Protein Ligases, Ubiquitination, Mitophagy, Ubiquitin-Specific Proteases

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PINK1/Parkin-mediated mitophagy in mammalian cells

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