ReviewMolecules and cells2012
PINK1 as a molecular checkpoint in the maintenance of mitochondrial function and integrity.
Review in Molecules and cells, 2012. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Evaluation of PINK1 protein expression as a predictive marker for the efficacy of adjuvant chemotherapy in colorectal cancer: a retrospective study.BMC gastroenterology · 2025Article
- The role of TRAP1 in regulating mitochondrial dynamics during acute hypoxia-induced brain injury.Journal of translational medicine · 2024Article
- Genetic and pharmacologic p32-inhibition rescue CHCHD2-linked Parkinson's disease phenotypes in vivo and in cell models.Journal of biomedical science · 2024Article
- Identification of Altered Blood MicroRNAs and Plasma Proteins in a Rat Model of Parkinson's Disease.Molecular neurobiology · 2022Article
- PINK1 Inhibits Multimeric Aggregation and Signaling of MAVS and MAVS-Dependent Lung Pathology.American journal of respiratory cell and molecular biology · 2021Article
- The Mitochondrial Hsp90 TRAP1 and Alzheimer's Disease.Frontiers in molecular biosciences · 2021Review
- PINK1 alleviates thermal hypersensitivity in a paclitaxel-induced Drosophila model of peripheral neuropathy.PloS one · 2020Article
- Sensory neuropathy and nociception in rodent models of Parkinson's disease.Disease models & mechanisms · 2019Review
- Isocitrate protects DJ-1 null dopaminergic cells from oxidative stress through NADP+-dependent isocitrate dehydrogenase (IDH).PLoS genetics · 2017Article
- Role of FOXO transcription factors in crosstalk between mitochondria and the nucleus.Journal of bioenergetics and biomembranes · 2017Review
- Tumor Necrosis Factor Receptor-associated Protein 1 (TRAP1) Mutation and TRAP1 Inhibitor Gamitrinib-triphenylphosphonium (G-TPP) Induce a Forkhead Box O (FOXO)-dependent Cell Protective Signal from Mitochondria.The Journal of biological chemistry · 2016Article
- Comparison of the structure, function and autophagic maintenance of mitochondria in nigrostriatal and tuberoinfundibular dopamine neurons.Brain research · 2015Article
- Emerging functional cross-talk between the Keap1-Nrf2 system and mitochondria.Journal of clinical biochemistry and nutrition · 2015Review
- Mitochondrial Dysfunction and α-Synuclein Synaptic Pathology in Parkinson's Disease: Who's on First?Parkinson's disease · 2015Review
- Beneficial Effects of AMP-Activated Protein Kinase Agonists in Kidney Ischemia-Reperfusion: Autophagy and Cellular Stress Markers.Nephron. Experimental nephrology · 2014Article
- 6-Hydroxydopamine impairs mitochondrial function in the rat model of Parkinson's disease: respirometric, histological, and behavioral analyses.Journal of neural transmission (Vienna, Austria : 1996) · 2014Article
- Oxidative stress is not a major contributor to somatic mitochondrial DNA mutations.PLoS genetics · 2014Article
- Interactions Between Hepatitis C Virus and Mitochondria: Impact on Pathogenesis and Innate Immunity.Current pathobiology reports · 2013Article
- Aconitase causes iron toxicity in Drosophila pink1 mutants.PLoS genetics · 2013Article
- Drosophila DJ-1 decreases neural sensitivity to stress by negatively regulating Daxx-like protein through dFOXO.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD), the most prevalent neurodegenerative movement disorder, is characterized by an age-dependent selective loss of dopaminergic (DA) neurons. Although most PD cases are sporadic, more than 20 responsible genes in familial cases were identified recently. Genetic studies using Drosophila models demonstrate that PINK1, a mitochondrial kinase encoded by a PD-linked gene PINK1, is critical for maintaining mitochondrial function and integrity. This suggests that mitochondrial dysfunction is the main cause of PD pathogenesis. Further genetic and cell biological studies revealed that PINK1 recruits Parkin, an E3 ubiquitin ligase encoded by another PD-linked gene parkin, to mitochondria and regulates the mitochondrial remodeling process via the Parkin-mediated ubiquitination of various mitochondrial proteins. PINK1 also directly phosphorylates the mitochondrial proteins Miro and TRAP1, subsequently inhibiting mitochondrial transport and mitochondrial oxidative damage, respectively. Moreover, recent Drosophila genetic analyses demonstrate that the neuroprotective molecules Sir2 and FOXO specifically complement mitochondrial dysfunction and DA neuron loss in PINK1 null mutants, suggesting that Sir2 and FOXO protect mitochondria and DA neurons downstream of PINK1. Collectively, these recent results suggest that PINK1 plays multiple roles in mitochondrial quality control by regulating its mitochondrial, cytosolic, and nuclear targets.
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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.