ArticleTraffic (Copenhagen, Denmark)2011
Alzheimer's disease-associated ubiquilin-1 regulates presenilin-1 accumulation and aggresome formation.
Article in Traffic (Copenhagen, Denmark), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 74 citations in OpenAlex.
- Intermediate filaments associate with aggresome-like structures in proteostressed C. elegans neurons and influence large vesicle extrusions as exophers.Nature communications · 2023Article
- HSV-1 cellular model reveals links between aggresome formation and early step of Alzheimer's disease.Translational psychiatry · 2023Review
- Copper homeostasis and the ubiquitin proteasome system.Metallomics : integrated biometal science · 2023Review
- Regulation of Neurodegeneration-associated Protein Fragments by the N-degron Pathways.Neurotoxicity research · 2022Review
- It's not just a phase; ubiquitination in cytosolic protein quality control.Biochemical Society transactions · 2021Review
- Ubiquilin proteins regulate EGFR levels and activity in lung adenocarcinoma cells.Journal of cellular biochemistry · 2021Article
- Article
- Structure, dynamics and functions of UBQLNs: at the crossroads of protein quality control machinery.The Biochemical journal · 2020Review
- Bayesian integrative analysis of epigenomic and transcriptomic data identifies Alzheimer's disease candidate genes and networks.PLoS computational biology · 2020Article
- A Comprehensive Review of Alzheimer's Association with Related Proteins: Pathological Role and Therapeutic Significance.Current neuropharmacology · 2020Review
- Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration.International journal of molecular sciences · 2019Review
- Emerging Signal Regulating Potential of Genistein Against Alzheimer's Disease: A Promising Molecule of Interest.Frontiers in cell and developmental biology · 2019Review
- Early Presymptomatic Changes in the Proteome of Mitochondria-Associated Membrane in the APP/PS1 Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2018Article
- Cdc48 and ubiquilins confer selective anterograde protein sorting and entry into the multivesicular body in yeast.Molecular biology of the cell · 2018Article
- PSEN1 Mutant iPSC-Derived Model Reveals Severe Astrocyte Pathology in Alzheimer's Disease.Stem cell reports · 2017Article
- Concordance of Several Subcellular Interactions Initiates Alzheimer's Dementia: Their Reversal Requires Combination Treatment.American journal of Alzheimer's disease and other dementias · 2017Review
- Reduced body weight gain in ubiquilin-1 transgenic mice is associated with increased expression of energy-sensing proteins.Physiological reports · 2017Article
- Association betweenInternational journal of clinical and experimental pathology · 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
- Proteins that mediate protein aggregation and cytotoxicity distinguish Alzheimer's hippocampus from normal controls.Aging cell · 2016Article
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Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
Abstract
The Alzheimer's disease (AD)-associated ubiquilin-1 regulates proteasomal degradation of proteins, including presenilin (PS). PS-dependent γ-secretase generates β-amyloid (Aβ) peptides, which excessively accumulate in AD brain. Here, we have characterized the effects of naturally occurring ubiquilin-1 transcript variants (TVs) on the levels and subcellular localization of PS1 and other γ-secretase complex components and subsequent γ-secretase function in human embryonic kidney 293, human neuroblastoma SH-SY5Y and mouse primary cortical cells. Full-length ubiquilin-1 TV1 and TV3 that lacks the proteasome-interaction domain increased full-length PS1 levels as well as induced accumulation of high-molecular-weight PS1 and aggresome formation. Accumulated PS1 colocalized with TV1 or TV3 in the aggresomes. Electron microscopy indicated that aggresomes containing TV1 or TV3 were targeted to autophagosomes. TV1- and TV3-expressing cells did not accumulate other unrelated proteasome substrates, suggesting that the increase in PS1 levels was not because of a general impairment of the ubiquitin-proteasome system. Furthermore, PS1 accumulation and aggresome formation coincided with alterations in Aβ levels, particularly in cells overexpressing TV3. These effects were not related to altered γ-secretase activity or PS1 binding to TV3. Collectively, our results indicate that specific ubiquilin-1 TVs can cause PS1 accumulation and aggresome formation, which may impact AD pathogenesis or susceptibility.
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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.