ArticleCellular and molecular neurobiology2014
The proteasome function reporter GFPu accumulates in young brains of the APPswe/PS1dE9 Alzheimer's disease mouse model.
Article in Cellular and molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Targeting Ubiquitin-Proteasome Pathway by Natural Products: Novel Therapeutic Strategy for Treatment of Neurodegenerative Diseases.Frontiers in physiology · 2020Pooled it
- RawNutrition research and practice · 2023Article
- Effects of Phenylethanoid Glycosides Extracted fromBioMed research international · 2021Article
- Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation.Free radical biology & medicine · 2021Article
- Priming the Proteasome to Protect against Proteotoxicity.Trends in molecular medicine · 2020Review
- Proteasome Activation as a New Therapeutic Approach To Target Proteotoxic Disorders.Journal of medicinal chemistry · 2019Review
- Genetic Pathways of Aging and Their Relevance in the Dog as a Natural Model of Human Aging.Frontiers in genetics · 2019Review
- Could a Common Mechanism of Protein Degradation Impairment Underlie Many Neurodegenerative Diseases?Journal of experimental neuroscience · 2018Article
- Enhanced Proteostasis in Post-ischemic Stroke Mouse Brains by Ubiquilin-1 Promotes Functional Recovery.Cellular and molecular neurobiology · 2017Article
- Immunoproteasome deficiency alters microglial cytokine response and improves cognitive deficits in Alzheimer's disease-like APPPS1 mice.Acta neuropathologica communications · 2017Article
- Reduced body weight gain in ubiquilin-1 transgenic mice is associated with increased expression of energy-sensing proteins.Physiological reports · 2017Article
- USP14 inhibitor attenuates cerebral ischemia/reperfusion-induced neuronal injury in mice.Journal of neurochemistry · 2017Article
- Overexpression of Ubiquilin-1 Alleviates Alzheimer's Disease-Caused Cognitive and Motor Deficits and Reduces Amyloid-β Accumulation in Mice.Journal of Alzheimer's disease : JAD · 2017Article
- Proteotoxicity and cardiac dysfunction.Circulation research · 2015Review
- The proteasome activity reporter GFP-Cl1 is degraded by autophagy in the aging model Podospora anserina.F1000Research · 2014Article
- The ubiquitin-proteasome system in neurodegenerative diseases: precipitating factor, yet part of the solution.Frontiers in molecular neuroscience · 2014Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD), the most common cause of dementia, is neuropathologically characterized by accumulation of insoluble fibrous inclusions in the brain in the form of intracellular neurofibrillary tangles and extracellular senile plaques. Perturbation of the ubiquitin-proteasome system (UPS) has long been considered an attractive hypothesis to explain the pathogenesis of AD. However, studies on UPS functionality with various methods and AD models have achieved non-conclusive results. To get further insight into UPS functionality in AD, we have crossed a well-documented APPswe/PS1dE9 AD mouse model with a UPS functionality reporter, GFPu, mouse expressing green fluorescence protein (GFP) fused to a constitutive degradation signal (CL-1) that facilitates its rapid turnover in conditions of a normal UPS. Our western blot results indicate that GFPu reporter protein was accumulated in the cortex and hippocampus, but not striatum in the APPswe/PS1dE9 AD mouse model at 4 weeks of age, which is confirmed by fluorescence microscopy and elevated levels of p53, an endogenous UPS substrate. In accordance with this, the levels of ubiquitinated proteins were elevated in the AD mouse model. These results suggest that UPS is either impaired or functionally insufficient in specific brain regions in the APPswe/PS1dE9 AD mouse model at a very young age, long before senile plaque formation and the onset of memory loss. These observations may shed new light on the pathogenesis of AD.
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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.