ArticleCell death & disease2019
Bcl-2-associated athanogene 5 (BAG5) regulates Parkin-dependent mitophagy and cell death.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 49 citations in OpenAlex.
- One BAG Does Not Fit All: Differences and Similarities of BAG Family Members in Mediating Central Nervous System Homeostasis.Biological psychiatry · 2025Review
- Mitochondrial Damage and Autophagy Dysregulation in Alzheimer's Disease: Mechanisms and Therapeutic Opportunities.Neurochemical research · 2025Review
- Mechanistic insights into promotion of non-small cell lung cancer by BAG5 using integrative multi-omics approaches.Frontiers in immunology · 2025Article
- Identification of mitochondrial ATP synthase as the cellular target of Ru-polypyridyl-National science review · 2024Article
- BetaZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Mitophagy-related regulated cell death: molecular mechanisms and disease implications.Cell death & disease · 2024Review
- High frequency electrical stimulation reduces α-synuclein levels and α-synuclein-mediated autophagy dysfunction.Scientific reports · 2024Article
- BAG5 regulates HSPA8-mediated protein folding required for sperm head-tail coupling apparatus assembly.EMBO reports · 2024Article
- Mechanism and role of mitophagy in the development of severe infection.Cell death discovery · 2024Review
- Human proteins curing yeast prions.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Low expression of PINK1 and PARK2 predicts poor prognosis in patients with esophageal squamous cell carcinoma.World journal of surgical oncology · 2023Article
- Identification of candidate mitochondrial inheritance determinants using the mammalian cell-free system.eLife · 2023Article
- BAG family proteins contributes to autophagy-mediated multidrug resistance of tumor.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Review
- Identification of BAG5 as a Potential Biomarker for Parkinson's Disease Patients With R492XFrontiers in neuroscience · 2022Article
- Role of BAG5 in Protein Quality Control: Double-Edged Sword?Frontiers in aging · 2022Review
- Precise control of mitophagy through ubiquitin proteasome system and deubiquitin proteases and their dysfunction in Parkinson's disease.BMB reports · 2021Article
- Review
- African Swine Fever Virus Protein E199L Promotes Cell Autophagy through the Interaction of PYCR2.Virologica Sinica · 2021Article
- Regulation of Parkin-dependent mitophagy by Bcl-2-associated athanogene (BAG) family members.Neural regeneration research · 2021Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
As pathogenic Parkin mutations result in the defective clearance of damaged mitochondria, Parkin-dependent mitophagy is thought to be protective against the dopaminergic neurodegeneration observed in Parkinson's disease. Recent studies, however, have demonstrated that Parkin can promote cell death in the context of severe mitochondrial damage by degrading the pro-survival Bcl-2 family member, Mcl-1. Therefore, Parkin may act as a 'switch' that can shift the balance between protective or pro-death pathways depending on the degree of mitochondrial damage. Here, we report that the Parkin interacting protein, Bcl-2-associated athanogene 5 (BAG5), impairs mitophagy by suppressing Parkin recruitment to damaged mitochondria and reducing the movement of damaged mitochondria into the lysosomes. BAG5 also enhanced Parkin-mediated Mcl-1 degradation and cell death following severe mitochondrial insult. These results suggest that BAG5 may regulate the bi-modal activity of Parkin, promoting cell death by suppressing Parkin-dependent mitophagy and enhancing Parkin-mediated Mcl-1 degradation.
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Registered trials
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