ArticlePloS one2013
Poly-Ub-substrate-degradative activity of 26S proteasome is not impaired in the aging rat brain.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- The proteostasis paradox: from systemic collapse in aging to pathway-specific addiction in prostate cancer.Frontiers in cell and developmental biology · 2026Review
- Article
- Neuronal Senescence in the Aged Brain.Aging and disease · 2023Review
- Comprehensive Analysis of Proteasomal Complexes in Mouse Brain Regions Detects ENO2 as a Potential Partner of the Proteasome in the Striatum.Cellular and molecular neurobiology · 2022Article
- Keeping synapses in shape: degradation pathways in the healthy and aging brain.Neuronal signaling · 2022Review
- Proteostasis Perturbations and Their Roles in Causing Sterile Inflammation and Autoinflammatory Diseases.Cells · 2022Review
- Advances in Proteasome Enhancement by Small Molecules.Biomolecules · 2021Review
- T-Type CaInternational journal of molecular sciences · 2021Article
- Proteasome Complexes and Their Heterogeneity in Colorectal, Breast and Pancreatic Cancers.Journal of Cancer · 2021Article
- Proteostasis Dysfunction in Aged Mammalian Cells. The Stressful Role of Inflammation.Frontiers in molecular biosciences · 2021Review
- Age-related memory deficits are associated with changes in protein degradation in brain regions critical for trace fear conditioning.Neurobiology of aging · 2020Article
- Large database for the analysis and prediction of spliced and non-spliced peptide generation by proteasomes.Scientific data · 2020Article
- Perturbations of Ubiquitin-Proteasome-Mediated Proteolysis in Aging and Alzheimer's Disease.Frontiers in aging neuroscience · 2019Review
- Immunoproteasome deficiency alters microglial cytokine response and improves cognitive deficits in Alzheimer's disease-like APPPS1 mice.Acta neuropathologica communications · 2017Article
- Life and death in the trash heap: The ubiquitin proteasome pathway and UCHL1 in brain aging, neurodegenerative disease and cerebral Ischemia.Ageing research reviews · 2017Review
- Iron Loading Selectively Increases Hippocampal Levels of Ubiquitinated Proteins and Impairs Hippocampus-Dependent Memory.Molecular neurobiology · 2016Article
- The Ubiquitin-Proteasome System and Molecular Chaperone Deregulation in Alzheimer's Disease.Molecular neurobiology · 2016Review
- Article
- Active Degradation Explains the Distribution of Nuclear Proteins during Cellular Senescence.PloS one · 2015Article
- A fine balance: Regulation of hippocampal Arc/Arg3.1 transcription, translation and degradation in a rat model of normal cognitive aging.Neurobiology of learning and memory · 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
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteostasis is critical for the maintenance of life. In neuronal cells an imbalance between protein synthesis and degradation is thought to be involved in the pathogenesis of neurodegenerative diseases during aging. Partly, this seems to be due to a decrease in the activity of the ubiquitin-proteasome system, wherein the 20S/26S proteasome complexes catalyse the proteolytic step. We have characterised 20S and 26S proteasomes from cerebrum, cerebellum and hippocampus of 3 weeks old (young) and 24 month old (aged) rats. Our data reveal that the absolute amount of the proteasome is not dfferent between both age groups. Within the majority of standard proteasomes in brain the minute amounts of immuno-subunits are slightly increased in aged rat brain. While this goes along with a decrease in the activities of 20S and 26S proteasomes to hydrolyse synthetic fluorogenic tripeptide substrates from young to aged rats, the capacity of 26S proteasomes for degradation of poly-Ub-model substrates and its activation by poly-Ub-substrates is not impaired or even slightly increased in brain of aged rats. We conclude that these alterations in proteasome properties are important for maintaining proteostasis in the brain during an uncomplicated aging process.
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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.