ArticleMolecular neurobiology2014
Presenilin-1 regulates the expression of p62 to govern p62-dependent tau degradation.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Autophagy and Cellular Senescence in Alzheimer's Disease: Key Drivers of Neurodegeneration.CNS neuroscience & therapeutics · 2025Review
- Carbonic anhydrase inhibition ameliorates tau toxicity via enhanced tau secretion.Nature chemical biology · 2025Article
- DUSP6 regulates Notch1 signalling in colorectal cancer.Nature communications · 2024Article
- Galectin-3 aggravates microglial activation and tau transmission in tauopathy.The Journal of clinical investigation · 2024Article
- Brain insulin resistance linked Alzheimer's and Parkinson's disease pathology: An undying implication of epigenetic and autophagy modulation.Inflammopharmacology · 2023Review
- Review
- Fighting the Cause of Alzheimer's and GNE Myopathy.Frontiers in neuroscience · 2018Review
- Alzheimer's Disease and Type 2 Diabetes: A Critical Assessment of the Shared Pathological Traits.Frontiers in neuroscience · 2018Review
- ErbB2 regulates autophagic flux to modulate the proteostasis of APP-CTFs in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Perspective Insights into Disease Progression, Diagnostics, and Therapeutic Approaches in Alzheimer's Disease: A Judicious Update.Frontiers in aging neuroscience · 2017Review
- G206D Mutation of Presenilin-1 Reduces Pen2 Interaction, Increases Aβ42/Aβ40 Ratio and Elevates ER Ca(2+) Accumulation.Molecular neurobiology · 2015Article
- Autophagy in Alzheimer's disease.Reviews in the neurosciences · 2015Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in presenilin-1 (PS1) are tightly associated with early-onset familial Alzheimer's disease (FAD), which is characterized by extracellular amyloid plaques and the accumulation of intracellular Tau. In addition to being the catalytic subunit of γ-secretase, PS1 has been shown to regulate diverse cellular functions independent of its proteolytic activity. We found that cells deficient in PS1 exhibit reduced levels of p62 protein, a cargo-receptor shuttling Tau for degradation. The downregulation of PS1 led to a significant decrease in both the protein and mRNA transcript of p62, concomitant with attenuated p62 promoter activity. This PS1-dependent regulation of p62 expression was mediated through an Akt/AP-1 pathway independent of the proteolytic activity of PS1/γ-secretase. This p62-mediated Tau degradation was significantly impaired in PS1-deficient cells, which can be rescued by ectopic expression of either p62 or wild-type PS1 but not mutant PS1 containing FAD-linked mutations. Our study suggests a novel function for PS1 in modulating p62 expression to control the proteostasis of Tau.
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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.