Overexpression of U1 snRNA induces decrease of U1 spliceosome function associated with Alzheimer's disease

Journal of Neurogenetics
Zhi ChengTao Zhang

Abstract

We recently reported that presenilin-1 (PS1) induced an increase of U1 snRNA expression accompanied with the change of amyloid precursor protein expression, β-amyloid level and cell death. In the present study, our data showed that both overexpression and knockdown of U1 snRNA could cause the loss in the function of U1 snRNA and resulted in PCPA as well as the same downstream phenomena including the expression changes of genes specific to AD, tau hyperphosphorylation on the site of Thr212, the decrease of acetylated α-tubulin, the reduction of cell viability and upregulation of RIPK1, RIPK3 and caspase8. These findings not only helped researchers better understand the functions of U1 snRNA, but also paved the way to reveal the mechanisms of AD from a different point of view and may find a new therapeutic target for the disease.

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Citations

May 11, 2018·Biochemical Society Transactions·Arlene M A GlasgowCatherine M Greene
Apr 10, 2018·Frontiers in Aging Neuroscience·Bing Bai
Nov 2, 2019·International Journal of Molecular Sciences·Virginie Bottero, Judith A Potashkin
Aug 5, 2020·Proceedings of the National Academy of Sciences of the United States of America·Weili WangYunfeng Liu

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