ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
PINK1 Content in Mitochondria is Regulated by ER-Associated Degradation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Inter-organellar Communication in Parkinson's and Alzheimer's Disease: Looking Beyond Endoplasmic Reticulum-Mitochondria Contact Sites.Frontiers in neuroscience · 2022Pooled it
- Mitophagy coordinates organelle crosstalk in health and diseases.Signal transduction and targeted therapy · 2026Review
- The PINK1-VCP-p47 pathway protects against tau-induced dendritic shrinkage in cortical neurons through interaction with STIP1.Neurobiology of disease · 2026Article
- Whole Blood Transcriptomic Analysis of Sickle Cell Trait.European journal of haematology · 2026Article
- Schisandrol B protects against lithocholic acid-induced cholestatic liver injury in mice through mitochondrial biogenesis.Chinese medicine · 2026Article
- The endoplasmic reticulum in mitochondrial protein targeting: A neuronal perspective on organelle crosstalk.Protein science : a publication of the Protein Society · 2026Review
- Parkin deficiency impairs female fertility, oocyte development, fertilization and mitochondrial function in mice.npj aging · 2026Article
- Physical exercise as a precision strategy for targeted PINK1 recruitment- a mechanistic review.Frontiers in physiology · 2026Review
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- The many faces of p97/Cdc48 in mitochondrial homeostasis.Essays in biochemistry · 2025Review
- Electron microscopy reveals saturated fatty acid-induced membrane defects in AdipoR2-depleted cells.Lipids in health and disease · 2025Article
- MYC affects mitochondrial function in IgA nephropathy by promoting the degradation of MFN1 through HRD1.Immunologic research · 2025Article
- Dynamic gene regulatory network inference from single-cell data using optimal transport.Bioinformatics (Oxford, England) · 2025Article
- Integrative Analysis of DNA Methylation and microRNA Reveals GNPDA1 and SLC25A16 Related to Biopsychosocial Factors Among Taiwanese Women with a Family History of Breast Cancer.Journal of personalized medicine · 2025Article
- A long-lived pool of PINK1 imparts a molecular memory of depolarization-induced activity.Science advances · 2025Article
- The interconnective role of the UPS and autophagy in the quality control of cancer mitochondria.Cellular and molecular life sciences : CMLS · 2025Review
- Organellar quality control crosstalk in aging-related disease: Innovation to pave the way.Aging cell · 2025Review
- Exercise regulates mitophagy to alleviate parkinsonian neurodegeneration.Frontiers in aging neuroscience · 2025Review
- Mitophagy related diagnostic biomarkers for coronary in-stent restenosis identified using machine learning and bioinformatics.Scientific reports · 2024Article
- Novel functions of the ER-located Hsp40s DNAJB12 and DNAJB14 on proteins at the outer mitochondrial membrane under stress mediated by CCCP.Molecular and cellular biochemistry · 2024Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 5 countries.
Funding
Abstract
Maintaining a pool of functional mitochondria requires degradation of damaged ones within the cell. PINK1 is critical in this quality-control process: loss of mitochondrial membrane potential causes PINK1 to accumulate on the mitochondrial surface, triggering mitophagy. However, little is known about how PINK1 is regulated. Recently, we showed that PINK1 content is kept low in healthy mitochondria by continuous ubiquitination and proteasomal degradation of its mature form via a mechanism inconsistent with the proposed N-end rule process. Using both human female and monkey cell lines, we now demonstrate that once generated within the mitochondria, 52 kDa PINK1 adopts a mitochondrial topology most consistent with it being at the mitochondrial-endoplasmic reticulum (ER) interface. From this particular submitochondrial location, PINK1 interacts with components of the ER-associated degradation pathway, such as the E3 ligases gp78 and HRD1, which cooperate to catalyze PINK1 ubiquitination. The valosin-containing protein and its cofactor, UFD1, then target ubiquitinated PINK1 for proteasomal degradation. Our data show that PINK1 in healthy mitochondria is negatively regulated via an interplay between mitochondria and ER, and shed light on how this mitochondrial protein gains access to the proteasome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.