ReviewJournal of neural transmission (Vienna, Austria : 1996)2017
Twenty years since the discovery of the parkin gene.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Genome-wide Burden of Rare Short Deletions Is Enriched in Major Depressive Disorder in Four Cohorts.Biological psychiatry · 2019Pooled it
- In vitro and in vivo rescue of dopaminergic neurons in Parkinson's disease models after Parkin gene therapy.Gene therapy · 2026Article
- High molecular weight insoluble parkin in the substantia nigra of patients with idiopathic Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Ozzy Osbourne and Parkinson's disease: from darkness to awareness.Arquivos de neuro-psiquiatria · 2026Article
- Neuronal guidance signaling in neurodegenerative diseases: Key regulators that function at neuron-glia and neuroimmune interfaces.Neural regeneration research · 2026Article
- Mitochondrial resilience: a convergent framework for pathogenesis and neuroprotection in Parkinson's disease.Frontiers in pharmacology · 2026Review
- Epigenetic and Transcriptomic Alterations of Protein Aggregation-Linked Genes in Suicide: A Pilot Study.Genes · 2025Article
- Parkinson Disease Signaling Pathways, Molecular Mechanisms, and Potential Therapeutic Strategies: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Parkinson's disease physiopathology-beyond theFrontiers in aging neuroscience · 2025Review
- In situ stoichiometry amounts of p62 and poly-ubiquitin exceed the increase of alpha-synuclein during degeneration of catecholamine cells induced by autophagy inhibition in vitro.Journal of neural transmission (Vienna, Austria : 1996) · 2024Article
- Activation of parkin by a molecular glue.Nature communications · 2024Article
- PRKN-linked familial Parkinson's disease: cellular and molecular mechanisms of disease-linked variants.Cellular and molecular life sciences : CMLS · 2024Review
- Is There a Place for Lewy Bodies before and beyond Alpha-Synuclein Accumulation? Provocative Issues in Need of Solid Explanations.International journal of molecular sciences · 2024Review
- Signaling pathways in Parkinson's disease: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Nanomedicine for Neurodegenerative Disorders: Focus on Alzheimer's and Parkinson's Diseases.International journal of molecular sciences · 2021Review
- Aberrant proteins expressed in skin fibroblasts of Parkinson's disease patients carrying heterozygous variants of glucocerebrosidase and parkin genes.Biomedical reports · 2021Article
- Interaction between Parkin andCells · 2021Review
- Potential of PINK1 and PARKIN Proteins as Biomarkers for Active Multiple Sclerosis: A Japanese Cohort Study.Frontiers in immunology · 2021Article
- Diffusion MRI Captures White Matter Microstructure Alterations in PRKN Disease.Journal of Parkinson's disease · 2021Article
- Dextromethorphan Dampens Neonatal Astrocyte Activation and Endoplasmic Reticulum Stress Induced by Prenatal Exposure to Buprenorphine.Behavioural neurology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nearly 20 years have passed since we identified the causative gene for a familial Parkinson's disease, parkin (now known as PARK2), in 1998. PARK2 is the most common gene responsible for young-onset Parkinson's disease. It codes for the protein Parkin RBR E3 ubiquitin-protein ligase (PARK2), which directly links to the ubiquitin-proteasome as a ubiquitin ligase. PARK2 is involved in mitophagy, which is a type of autophagy, in collaboration with PTEN-induced putative kinase 1 (PINK1). The PINK1 gene (previously known as PARK6) is also a causative gene for young-onset Parkinson's disease. Both gene products may be involved in regulating quality control within the mitochondria. The discovery of PARK2 as a cause of young-onset Parkinson's disease has had a major impact on other neurodegenerative diseases. The involvement of protein degradation systems has been implicated as a common mechanism for neurodegenerative diseases in which inclusion body formation is observed. The discovery of the involvement of PARK2 in Parkinson's disease focused attention on the involvement of protein degradation systems in neurodegenerative diseases. In this review, we focus on the history of the discovery of PARK2, the clinical phenotypes of patients with PARK2 mutations, and its functional roles.
Indexed as
Identifiers
What OpenQuestion holds
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.