ArticleCell death & disease2014
Inhibition of apoptotic Bax translocation to the mitochondria is a central function of parkin.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- TMBIM6 enhances dopaminergic neuron survival by modulating the IRE1a pathway in Parkinson's disease.Cell death & disease · 2026Article
- Parkin protects against traumatic brain injury through regulating mitochondrial quality control.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Activation of endogenous PRKN by structural derepression is linked to increased turnover of the E3 ubiquitin ligase.Autophagy · 2025Article
- Different amyloid β42 preparations induce different cell death pathways in the model of SH-SY5Y neuroblastoma cells.Cellular & molecular biology letters · 2024Article
- Mitochondria and cell death.Nature cell biology · 2024Review
- The Potentiality of Natural Products and Herbal Medicine as Novel Medications for Parkinson's Disease: A Promising Therapeutic Approach.International journal of molecular sciences · 2024Review
- Ailanthone blocks mitophagy to promote mtDNA leakage through BAX-BAK1 pores and suppress hepatocellular carcinoma cell proliferation.Frontiers in pharmacology · 2024Article
- Ubiquitin-proteasome pathway-mediated regulation of the Bcl-2 family: effects and therapeutic approaches.Haematologica · 2024Review
- The E3 ubiquitin ligase TRIM17 promotes gastric cancer survival and progression via controlling BAX stability and antagonizing apoptosis.Cell death and differentiation · 2023Article
- Regulation of apoptosis by ubiquitination in liver cancer.American journal of cancer research · 2023Review
- The Links between Parkinson's Disease and Cancer.Biomedicines · 2020Review
- Modeling the function of BAX and BAK in early human brain development using iPSC-derived systems.Cell death & disease · 2020Article
- KPC1 alleviates hypoxia/reoxygenation-induced apoptosis in rat cardiomyocyte cells though BAX degradation.Journal of cellular physiology · 2019Article
- Parkin interacting substrate zinc finger protein 746 is a pathological mediator in Parkinson's disease.Brain : a journal of neurology · 2019Article
- Parkin overexpression protects from ageing-related loss of muscle mass and strength.The Journal of physiology · 2019Article
- Parkin Interacts with Apoptosis-Inducing Factor and Interferes with Its Translocation to the Nucleus in Neuronal Cells.International journal of molecular sciences · 2019Article
- Parkin inhibits BAK and BAX apoptotic function by distinct mechanisms during mitophagy.The EMBO journal · 2019Article
- PARK2 Suppresses Proliferation and Tumorigenicity in Non-small Cell Lung Cancer.Frontiers in oncology · 2019Article
- Neuronal Cell Death.Physiological reviews · 2018Review
- Vulnerable Parkin Loss-of-FunctionFrontiers in cellular neuroscience · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder, affecting 1-3% of the population over 65. Mutations in the ubiquitin E3 ligase parkin are the most common cause of autosomal recessive PD. The parkin protein possesses potent cell-protective properties and has been mechanistically linked to both the regulation of apoptosis and the turnover of damaged mitochondria. Here, we explored these two functions of parkin and the relative scale of these processes in various cell types. While biochemical analyses and subcellular fractionation were sufficient to observe robust parkin-dependent mitophagy in immortalized cells, higher resolution techniques appear to be required for primary culture systems. These approaches, however, did affirm a critical role for parkin in the regulation of apoptosis in primary cultured neurons and all other cells studied. Our prior work demonstrated that parkin-dependent ubiquitination of endogenous Bax inhibits its mitochondrial translocation and can account for the anti-apoptotic effects of parkin. Having found a central role for parkin in the regulation of apoptosis, we further investigated the parkin-Bax interaction. We observed that the BH3 domain of Bax is critical for its recognition by parkin, and identified two lysines that are crucial for parkin-dependent regulation of Bax translocation. Last, a disease-linked mutation in parkin failed to influence Bax translocation to mitochondria after apoptotic stress. Taken together, our data suggest that regulation of apoptosis by the inhibition of Bax translocation is a prevalent physiological function of parkin regardless of the kind of cell stress, preventing overt cell death and supporting cell viability during mitochondrial injury and repair.
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