ArticleJournal of molecular neuroscience : MN2017
A Preliminary Study: PS1 Increases U1 snRNA Expression Associated with AD.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Astrocyte-driven small vessel disease is an early, amyloid-independent feature of PSEN1 E280A familial Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Case study of a 47-year-old long COVID patient diagnosed with Alzheimer's disease.Quantitative imaging in medicine and surgery · 2025Article
- Autophagy regulation by RNA alternative splicing and implications in human diseases.Nature communications · 2022Review
- U1 snRNA over-expression affects neural oscillations and short-term memory deficits in mice.Cognitive neurodynamics · 2019Article
- Linking Endoplasmic Reticular Stress and Alternative Splicing.International journal of molecular sciences · 2018Review
- RNA Splicing in the Transition from B Cells to Antibody-Secreting Cells: The Influences of ELL2, Small Nuclear RNA, and Endoplasmic Reticulum Stress.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- U1 snRNP Alteration and Neuronal Cell Cycle Reentry in Alzheimer Disease.Frontiers in aging neuroscience · 2018Review
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
U1 small nuclear RNA (snRNA) is selectively enriched in 100% of familial Alzheimer's disease (AD) resulting from presenilin1 (PS1) and amyloid precursor protein (APP) mutations. However, it remains unknown what gene or protein cause the U1 snRNA overexpression and then resulted in AD. Using SH-SY5Y cells, we discovered that PS1 induced the overexpression of U1 snRNA, which increased the production of Aβ. Moreover, the U1 snRNA overexpression induced the upregulation of apoe and clu transcripts. In addition, the levels of phosphorylation of tau protein at Thr212 were significantly elevated in U1 snRNA overexpression cells. Immunofluorescence using antibodies reactive with the phosphorylation of tau at Thr212 site demonstrated the hyperphosphorylated tau localization with α-tubulin, the main component of cytoskeleton. Importantly, the increased levels of Bax, Bcl2, and Bax/Bcl2 ratio showed that the overexpression of U1 snRNA could cause cell apoptosis. Conclusively, these findings suggest that PS1 considerably increases the level of U1snRNA accompanied with the adverse change of Aβ level, AD-related tau cytoskeletal pathology, and cell apoptosis.
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Registered trials
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