ATAD3B is a mitophagy receptor mediating clearance of oxidative stress‐induced damaged mitochondrial DNA-Reference-Cited by-同舟云学术

ATAD3B is a mitophagy receptor mediating clearance of oxidative stress‐induced damaged mitochondrial DNA

Published:2021-03-05 Issue:8 Volume:40 Page:
ISSN:0261-4189
Container-title:The EMBO Journal
language:en
Short-container-title:EMBO J

Author:

Shu Li¹^ORCID,Hu Chao¹,Xu Meng¹,Yu Jianglong¹,He He¹,Lin Jie²,Sha Hongying³,Lu Bin⁴,Engelender Simone⁵,Guan Minxin⁶,Song Zhiyin¹^ORCID

Affiliation:

1. Hubei Key Laboratory of Cell Homeostasis College of Life Sciences Frontier Science Center for Immunology and Metabolism Wuhan University Wuhan China

2. Department of Neurology Huashan Hospital Fudan University Shanghai China

3. State Key Laboratory of Medical Neurobiology Institute of Brain Science Shanghai Medical College Fudan University Shanghai China

4. Attardi Institute of Mitochondrial Biomedicine School of Life Sciences Wenzhou Medical University Wenzhou China

5. Department of Biochemistry Rappaport Faculty of Medicine Technion‐Israel Institute of Technology Haifa Israel

6. Institute of Genetics Zhejiang University School of Medicine Hangzhou China

Funder

National Natural Science Foundation of China

Ministry of Science and Technology of the People's Republic of China

Publisher

EMBO

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology,General Neuroscience

Link

https://onlinelibrary.wiley.com/doi/pdf/10.15252/embj.2020106283

Reference58 articles.

1. Mitochondrial DNA damage is a hallmark of chemically induced and the R6/2 transgenic model of Huntington's disease

2. The Maintenance of Mitochondrial DNA Integrity--Critical Analysis and Update

3. Specific elimination of mutant mitochondrial genomes in patient-derived cells by mitoTALENs

4. ATAD3 proteins: brokers of a mitochondria-endoplasmic reticulum connection in mammalian cells

5. UVC-Induced Mitochondrial Degradation via Autophagy Correlates with mtDNA Damage Removal in Primary Human Fibroblasts

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