How it all Started: Tau and Protein Phosphatase 2A

被引：28
|
作者：
Liu, Chang [1 ]
Goetz, Juergen [1 ,2 ]
机构：
[1] Univ Sydney, Brain & Mind Res Inst, Camperdown, NSW, Australia
[2] Univ Queensland, QBI, CADR, Brisbane, Qld 4072, Australia
来源：
JOURNAL OF ALZHEIMERS DISEASE | 2013年 / 37卷 / 03期
基金：
英国医学研究理事会; 澳大利亚研究理事会;
关键词：
Alzheimer's disease; frontotemporal dementia; nucleus; protein phosphatase 2A; SFPQ; tau; transcription factor; PAIRED HELICAL FILAMENTS; ACTIVATING-FACTOR-I; FRONTOTEMPORAL LOBAR DEGENERATION; MICROTUBULE-ASSOCIATED PROTEIN-2; ALZHEIMER-DISEASE; NEUROFIBRILLARY TANGLES; ABNORMAL PHOSPHORYLATION; CHROMOSOMAL LOCALIZATION; DEVELOPMENTAL REGULATION; ANTIGENIC DETERMINANTS;
D O I：
10.3233/JAD-130503
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
This review is dedicated to Inge Grundke-Iqbal who laid the foundations of the tau field, by isolating tau from the Alzheimer's disease (AD) brain, discovering that tau is hyperphosphorylated, and proving a critical role of protein phosphatase 2A (PP2A) and its endogenous inhibitor I-2 (PP2A) in this process. This memorial starts with a few personal notes, and then covers how subcellular fractionation helped in isolating tau. We review in detail the role of PP2A and its endogenous inhibitor in tau phosphorylation. We discuss the role that methylation and phosphorylation have in regulating PP2A activity. We add what we have contributed to understanding the role of tau and PP2A in AD using PP2A transgenic and knockout models, and conclude by addressing two underexplored areas in tau research: tau's non-canonical functions and the role distinct tau isoforms have in a physiological context.
引用
收藏
页码：483 / 494
页数：12
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