Tau splicing and the intricacies of dementia

被引：57

作者：

Andreadis, Athena ^{[1
]}

机构：

[1] Univ Massachusetts, Sch Med, Dept Cell Biol, Worcester, MA 01655 USA

来源：

JOURNAL OF CELLULAR PHYSIOLOGY | 2012年 / 227卷 / 03期

关键词：

PROXIMAL DOWNSTREAM INTRON; MYOTONIC-DYSTROPHY TYPE-1; ALZHEIMERS-DISEASE; NEURODEGENERATIVE DISEASES; FRONTOTEMPORAL DEMENTIA; GENE-EXPRESSION; EXON; 10; PROTEIN-TAU; TAUOPATHIES; MUTATIONS;

D O I：

10.1002/jcp.22842

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Tau is a microtubule-associated protein that fulfills several functions critical for neuronal formation and health. Tau discharges its functions by producing multiple isoforms via regulated alternative splicing. These isoforms modulate tau function in normal brain by altering the domains of the protein, thereby influencing its localization, conformation, and post-translational modifications and hence its availability and affinity for microtubules and other ligands. Disturbances in tau expression result in disruption of the neuronal cytoskeleton and formation of tau structures (neurofibrillary tangles) found in brains of dementia sufferers. More specifically, aberrations in tau splicing regulation directly cause several neurodegenerative diseases, which lead to dementia. In this review, I present our cumulative knowledge of tau splicing regulation in connection with neurodegeneration and also briefly go over the still-extensive list of questions that are connected to tau (dys)function. J. Cell. Physiol. 227: 12201225, 2012. (C) 2011 Wiley Periodicals, Inc.

引用

页码：1220 / 1225

页数：6

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