RNA剪接
疾病
信号
核糖核酸
生物
神经科学
RNA结合蛋白
计算生物学
医学
遗传学
细胞生物学
病理
基因
作者
Flora Cheng,Tyler Chapman,S. Zhang,Marco Morsch,Roger S. Chung,Albert Lee,Stephanie L. Rayner
标识
DOI:10.1016/j.arr.2024.102246
摘要
TAR DNA binding protein-43 (TDP-43) is a key component in RNA splicing which plays a crucial role in the aging process. In neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Limbic-predominant age-related TDP-43 Encephalopathy (LATE), TDP-43 can be mutated, mislocalised out of the nucleus of neurons and glial cells and form cytoplasmic inclusions. These TDP-43 alterations can lead to its RNA splicing dysregulation and contribute to mis-splicing of various types of RNA, such as mRNA, microRNA, and circRNA. These changes can result in the generation of an altered transcriptome and proteome within cells, ultimately changing the diversity and quantity of gene products. In this review, we summarise the findings of novel atypical RNAs resulting from TDP-43 dysfunction and their potential biomarkers or targets for therapeutic development.
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