ReviewNeuromolecular medicine2003
Parkin's substrates and the pathways leading to neuronal damage.
Review in Neuromolecular medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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.
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Who cites it
24 citing papers in PubMed, 51 citations in OpenAlex.
- Interactions of VMAT2 with CDCrel-1 and Parkin in Methamphetamine Neurotoxicity.International journal of molecular sciences · 2024Article
- Neurotoxic Methamphetamine Doses Alter CDCel-1 Levels and Its Interaction with Vesicular Monoamine Transporter-2 in Rat Striatum.bioRxiv : the preprint server for biology · 2024Article
- Animal Models of Autosomal Recessive Parkinsonism.Biomedicines · 2021Review
- Maackiain Ameliorates 6-Hydroxydopamine andInternational journal of molecular sciences · 2020Article
- Impact of altered phosphorylation on loss of function of juvenile Parkinsonism-associated genetic variants of the E3 ligase parkin.The Journal of biological chemistry · 2018Article
- Carnosic Acid Attenuates 6-Hydroxydopamine-Induced Neurotoxicity in SH-SY5Y Cells by Inducing Autophagy Through an Enhanced Interaction of Parkin and Beclin1.Molecular neurobiology · 2017Article
- Computational identification and analysis of neurodegenerative disease associated protein kinases in hominid genomes.Genes & diseases · 2016Article
- Mitochondrial Quality Control via the PGC1α-TFEB Signaling Pathway Is Compromised by Parkin Q311X Mutation But Independently Restored by Rapamycin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Parkin loss leads to PARIS-dependent declines in mitochondrial mass and respiration.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Parkin-mediated ubiquitination of mutant glucocerebrosidase leads to competition with its substrates PARIS and ARTS.Orphanet journal of rare diseases · 2014Article
- Parkin plays a role in sporadic Parkinson's disease.Neuro-degenerative diseases · 2014Review
- Parthanatos mediates AIMP2-activated age-dependent dopaminergic neuronal loss.Nature neuroscience · 2013Article
- Mutation in E1, the ubiquitin activating enzyme, reduces Drosophila lifespan and results in motor impairment.PloS one · 2013Article
- Mitochondrial dysfunction precedes other sub-cellular abnormalities in an in vitro model linked with cell death in Parkinson's disease.Neurotoxicity research · 2012Article
- Modification by ubiquitin-like proteins: significance in apoptosis and autophagy pathways.International journal of molecular sciences · 2012Review
- Macroautophagy and the proteasome are differently involved in the degradation of alpha-synuclein wild type and mutated A30P in an in vitro inducible model (PC12/TetOn).Neuroscience · 2011Article
- The Unfolded Protein Response, Degradation from Endoplasmic Reticulum and Cancer.Genes & cancer · 2010Article
- Parkin deficiency disrupts calcium homeostasis by modulating phospholipase C signalling.The FEBS journal · 2009Article
- Parkin expression profile in dopamine d3 receptor knock-out mice brains.Neurochemical research · 2009Article
- The PINK1/Parkin pathway regulates mitochondrial morphology.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Mutations in the Parkin gene are associated with Parkinson s disease (PD). The gene product has been shown to be an E3 protein-ubiquitin ligase, catalyzing the addition of ubiquitin to target proteins prior to their destruction via the proteasome. This activity is thus key in regulating the turnover of substrate proteins. A predictive hypothesis for how this results in PD is that the misregulation of proteasomal degradation of Parkin s substrates is deleterious to neurons. Several different laboratories have identified alternate candidate proteins. In this review, the likelihood of each of the proposed substrates for parkin being robust will be evaluated. The distribution and abundance of the proteins will be examined for clues as to which are the pathologically important substrates for parkin. The possibility that loss of regulation of turnover of one or more of these substrates contributes to the selective neurodegeneration seen in PD is also discussed.
Indexed as
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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.