ReviewEMBO reports2004
How does parkin ligate ubiquitin to Parkinson's disease?
Review in EMBO reports, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses 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
46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 130 citations in OpenAlex.
- Mapping the research of mitochondria and Parkinson's disease: a bibliometric analysis.Frontiers in neurology · 2024Pooled it
- Genome-wide association analysis of coffee drinking suggests association with CYP1A1/CYP1A2 and NRCAM.Molecular psychiatry · 2012Pooled it
- Proteasome Dysregulation in Parkinson's Disease: Insights from Blood-Based Analyses.Molecular neurobiology · 2025Article
- Unraveling neuroprotection in Parkinson's disease: Nrf2-Keap1 pathway's vital role amidst pathogenic pathways.Inflammopharmacology · 2024Review
- Dynamic control of the dopamine transporter in neurotransmission and homeostasis.NPJ Parkinson's disease · 2021Review
- Autophagy in Parkinson's Disease.Journal of molecular biology · 2020Review
- Elucidating Critical Proteinopathic Mechanisms and Potential Drug Targets in Neurodegeneration.Cellular and molecular neurobiology · 2020Review
- Article
- Parkin Mutation Affects Clock Gene-Dependent Energy Metabolism.International journal of molecular sciences · 2019Article
- Increased Levels of cAMP by the Calcium-Dependent Activation of Soluble Adenylyl Cyclase inCells · 2019Article
- Parkin in Parkinson's Disease and Cancer: a Double-Edged Sword.Molecular neurobiology · 2018Review
- Characterization of Dopaminergic System in the Striatum of Young Adult Park2Scientific reports · 2018Article
- Parkin targets HIF-1α for ubiquitination and degradation to inhibit breast tumor progression.Nature communications · 2017Article
- Parkin-phosphoubiquitin complex reveals cryptic ubiquitin-binding site required for RBR ligase activity.Nature structural & molecular biology · 2017Article
- PINK1, Parkin, and Mitochondrial Quality Control: What can we Learn about Parkinson's Disease Pathobiology?Journal of Parkinson's disease · 2017Review
- Versatile members of the DNAJ family show Hsp70 dependent anti-aggregation activity on RING1 mutant parkin C289G.Scientific reports · 2016Article
- Linking F-box protein 7 and parkin to neuronal degeneration in Parkinson's disease (PD).Molecular brain · 2016Review
- Parkin promotes proteasomal degradation of p62: implication of selective vulnerability of neuronal cells in the pathogenesis of Parkinson's disease.Protein & cell · 2016Article
- Relationships between diabetes and cognitive impairment.Endocrinology and metabolism clinics of North America · 2014Review
- Behavioral phenotyping of Parkin-deficient mice: looking for early preclinical features of Parkinson's disease.PloS one · 2014Article
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
Recessive mutations in the human PARKIN gene are the most common cause of hereditary parkinsonism, which arises from the degeneration of dopaminergic neurons in the substantia nigra. However, the molecular mechanisms by which the loss of parkin causes dopaminergic neurodegeneration are not well understood. Parkin is an enzyme that ubiquitinates several candidate substrate proteins and thereby targets them for proteasomal degradation. Hypothesis-driven searches have led to the discovery of aggregation-prone protein substrates of parkin. Moreover, the enzyme is upregulated when under unfolded protein stress. Thus, loss-of-function mutations of parkin might impair the removal of potentially toxic protein aggregates. However, the limited neuropathological information that is available from parkin-proven patients, as well as the recent knockout of the parkin gene in fruit flies and mice, may indicate a more complex disease mechanism, possibly involving the misfolding of parkin itself or of additional substrates. The risk factors that predispose dopaminergic neurons to degenerate on parkin failure are yet to be identified.
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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.