ReviewMolecular neurobiology2004
Linkage between the proteasome pathway and neurodegenerative diseases and aging.
Review in Molecular neurobiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Trial
- Impact of severe hypoglycemia on the heat shock and related protein response.Scientific reports · 2021Trial
- Oxidative Stress Markers and Heat Shock Proteins in Non-Obese Women with Polycystic Ovary Syndrome Are Not Elevated and Show No Correlation with Vitamin D.Biomedicines · 2023Article
- Hypoglycemia Impairs the Heat Shock Protein Response: A Risk for Heat Shock in Cattle?Frontiers in veterinary science · 2022Article
- Design and evaluation of bi-functional iron chelators for protection of dopaminergic neurons from toxicants.Archives of toxicology · 2020Article
- Proteasome Activation as a New Therapeutic Approach To Target Proteotoxic Disorders.Journal of medicinal chemistry · 2019Review
- Could a Common Mechanism of Protein Degradation Impairment Underlie Many Neurodegenerative Diseases?Journal of experimental neuroscience · 2018Article
- Senescence-accelerated Mice (SAMs) as a Model for Brain Aging and Immunosenescence.Aging and disease · 2011Article
- Ubiquitin C-terminal hydrolase-l1 activity induces polyubiquitin accumulation in podocytes and increases proteinuria in rat membranous nephropathy.The American journal of pathology · 2011Article
- Comparison of rat liver and brain proteasomes for oxidative stress-induced inactivation: Influence of ageing and dietary restriction.Free radical research · 2009Article
- Redox proteomics in some age-related neurodegenerative disorders or models thereof.NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics · 2006Review
- MPTP and SNpc DA neuronal vulnerability: role of dopamine, superoxide and nitric oxide in neurotoxicity. Minireview.Neurotoxicity research · 2005Review
- Neuroprotection resulting from insufficiency of RANBP2 is associated with the modulation of protein and lipid homeostasis of functionally diverse but linked pathways in response to oxidative stress.Disease models & mechanismsArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During aging, the production of free radicals increases. This can result in damage to protein, the accumulation of which is characteristic of the aging process. This questions the efficacy of proteolytic systems. Among these systems, the proteasome and the adenosine triphosphate-ubiquitin-dependent pathway have been shown to play an important role in the elimination of abnormal proteins. There are two major steps in the ubiquitin-proteasome pathway: the conjugation of a polyubiquitin degradation signal to the substrate and the subsequent degradation of the tagged protein by the 26S proteasome. The 26S proteasome is build-up from the 20S proteasome, which is a cylinder-shaped multimeric complex, and two additional 19S complexes. The 20S proteasome can also bind to 11S regulator and is then implicated in antigen presentation. These regulators confer a high adaptability on proteasome. With advancing age, predisposition to neurodegenerative diseases increases. These diseases are also characterized by protein aggregation. Several findings such as the presence of ubiquinated proteins, usually broken down by proteasomes, and genetic anomalies involving the ubiquitin-proteasome system (parkin, UCH-L1) suggest a link between the ubiquitin-proteasome pathway and the genesis of these diseases.
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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.