ArticleCell death and differentiation2018
Analysis of neuronal phosphoproteome reveals PINK1 regulation of BAD function and cell death.
Article in Cell death and differentiation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Species-dependent activities of the PINK1-parkin axis.Translational neurodegeneration · 2026Review
- PINK1 functions in mitophagy and mitochondrial homeostasis during mice oocyte maturation.Cell & bioscience · 2025Article
- Role of mitophagy in breast cancer: mitophagy-apoptosis balance and reactive oxygen species play determining role.Frontiers in physiology · 2025Review
- SARS-CoV-2 membrane protein induces neurodegeneration via affecting Golgi-mitochondria interaction.Translational neurodegeneration · 2024Article
- Mitophagy-related regulated cell death: molecular mechanisms and disease implications.Cell death & disease · 2024Review
- Neurotropic virus infection and neurodegenerative diseases: Potential roles of autophagy pathway.CNS neuroscience & therapeutics · 2024Review
- Comparative analysis of primate and pig cells reveals primate-specific PINK1 expression and phosphorylation.Zoological research · 2024Article
- Kinase signalling adaptation supports dysfunctional mitochondria in disease.Frontiers in molecular biosciences · 2024Review
- Mitochondria in health, disease, and aging.Physiological reviews · 2023Review
- Integrated proteome and phosphoproteome analysis of gastric adenocarcinoma reveals molecular signatures capable of stratifying patient outcome.Molecular oncology · 2023Article
- Post-translational modification and mitochondrial function in Parkinson's disease.Frontiers in molecular neuroscience · 2023Review
- Regulation of reactive oxygen species on the mitophagy of human periodontal ligament cells through the PINK1/Parkin pathway under starvation.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2022Article
- PINK1 ameliorates acute-on-chronic liver failure by inhibiting apoptosis through mTORC2/AKT signaling.Cell death discovery · 2022Article
- PINK1 kinase dysfunction triggers neurodegeneration in the primate brain without impacting mitochondrial homeostasis.Protein & cell · 2022Article
- Mitochondrial Dysfunction Pathway Alterations Offer Potential Biomarkers and Therapeutic Targets for Ovarian Cancer.Oxidative medicine and cellular longevity · 2022Review
- Regulation of mitochondrial cargo-selective autophagy by posttranslational modifications.The Journal of biological chemistry · 2021Review
- Mitochondrial CaCell death & disease · 2021Article
- Systems Pharmacology-Based Dissection of Anti-Cancer Mechanism of Traditional Chinese HerbFrontiers in pharmacology · 2021Article
- Bis(zinc(II)-dipicolylamine)-functionalized sub-2 μm core-shell microspheres for the analysis of N-phosphoproteome.Nature communications · 2020Article
- PINK1 phosphorylates Drp1EMBO reports · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PINK1 mutations that disrupt its kinase activity cause autosomal recessive early onset Parkinson's disease (PD). Although research in recent years has elucidated a PINK1-Parkin pathway of mitophagy activation that requires PINK1 kinase activity, mitophagy-independent functions of PINK1 and their possible roles in PD pathogenesis have been proposed. Using an unbiased quantitative mass spectrometry approach to analyze the phosphoproteome in primary neurons from wild type and Pink1 knockout mice after mitochondrial depolarization, we uncovered PINK1-regulated phosphorylation sites, which involve coordinated activation of multiple signaling pathways that control cellular response to stress. We further identified the pro-apoptotic protein BAD as a potential mitochondrial substrate of PINK1 both in vitro and in vivo, and found that cells more susceptible to a12poptosis induced by mitochondrial damage can be rescued by phosphorylation mimic BAD. Our results thus suggest that PINK1 kinase activity is important for pro-apoptotic protein function in regulation of cell death.
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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.