Phosphorylation of microtubule-associated protein tau by isoforms of c-Jun N-terminal kinase (JNK)

被引:152
作者
Yoshida, H
Hastie, CJ
McLauchlan, H
Cohen, P
Goedert, M
机构
[1] MRC, Mol Biol Lab, Cambridge CB2 2QH, England
[2] Univ Dundee, Sch Life Sci, Div Signal Transduct Therapy, Dundee, Scotland
[3] Univ Dundee, Sch Life Sci, MRC, Prot Phosphorylat Unit, Dundee, Scotland
关键词
c-Jun N-terminal kinase; stress-activated protein kinase; tauopathy; tau protein;
D O I
10.1111/j.1471-4159.2004.02479.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Microtubule-associated protein tau in a hyperphosphorylated state is the major component of the filamentous lesions that define a number of neurodegenerative diseases commonly referred to as tauopathies. Hyperphosphorylation of tau at most sites appears to precede filament assembly. Many of the hyperphosphorylated sites are serine/threonine-proline sequences. Here we show that c-Jun N-terminal kinases JNK1, JNK2 and JNK3 phosphorylate tau at many serine/threonine-prolines, as assessed by the generation of the epitopes of phosphorylation-dependent anti-tau antibodies. Of the three protein kinases, JNK2 phosphorylated the most sites in tau, followed by JNK3 and JNK1. Phosphorylation by JNK isoforms resulted in a greatly reduced ability of tau to promote microtubule assembly. These findings extend the number of candidate protein kinases for the hyperphosphorylation of tau in Alzheimer's disease and other neurodegenerative disorders.
引用
收藏
页码:352 / 358
页数:7
相关论文
共 50 条
[1]  
Allen B, 2002, J NEUROSCI, V22, P9340
[2]   Activation of the JNK/p38 pathway occurs in diseases characterized by tau protein pathology and is related to tau phosphorylation but not to apoptosis [J].
Atzori, C ;
Ghetti, B ;
Piva, R ;
Srinivasan, AN ;
Zolo, P ;
Delisle, MB ;
Mirra, SS ;
Migheli, A .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2001, 60 (12) :1190-1197
[3]   ABNORMAL ALZHEIMER-LIKE PHOSPHORYLATION OF TAU-PROTEIN BY CYCLIN-DEPENDENT KINASES CDK2 AND CDK5 [J].
BAUMANN, K ;
MANDELKOW, EM ;
BIERNAT, J ;
PIWNICAWORMS, H ;
MANDELKOW, E .
FEBS LETTERS, 1993, 336 (03) :417-424
[4]   ABNORMAL TAU-PHOSPHORYLATION AT SER(396) IN ALZHEIMERS-DISEASE RECAPITULATES DEVELOPMENT AND CONTRIBUTES TO REDUCED MICROTUBULE-BINDING [J].
BRAMBLETT, GT ;
GOEDERT, M ;
JAKES, R ;
MERRICK, SE ;
TROJANOWSKI, JQ ;
LEE, VMY .
NEURON, 1993, 10 (06) :1089-1099
[5]   Phosphorylation of micro tubule-associated protein tau by stress-activated protein kinases in intact cells [J].
Buée-Scherrer, V ;
Goedert, M .
FEBS LETTERS, 2002, 515 (1-3) :151-154
[6]   AD2, a phosphorylation-dependent monoclonal antibody directed against tau proteins found in Alzheimer's disease [J].
BueeScherrer, V ;
Condamines, O ;
MourtonGilles, C ;
Jakes, R ;
Goedert, M ;
Pau, B ;
Delacourte, A .
MOLECULAR BRAIN RESEARCH, 1996, 39 (1-2) :79-88
[7]   MITOGEN ACTIVATED PROTEIN (MAP) KINASE TRANSFORMS TAU-PROTEIN INTO AN ALZHEIMER-LIKE STATE [J].
DREWES, G ;
LICHTENBERGKRAAG, B ;
DORING, F ;
MANDELKOW, EM ;
BIERNAT, J ;
GORIS, J ;
DOREE, M ;
MANDELKOW, E .
EMBO JOURNAL, 1992, 11 (06) :2131-2138
[8]   Effects of frontotemporal dementia FTDP-17 mutations on heparin-induced assembly of tau filaments [J].
Goedert, M ;
Jakes, R ;
Crowther, RA .
FEBS LETTERS, 1999, 450 (03) :306-311
[9]   Phosphorylation of microtubule-associated protein tau by stress-activated protein kinases [J].
Goedert, M ;
Hasegawa, M ;
Jakes, R ;
Lawler, S ;
Cuenda, A ;
Cohen, P .
FEBS LETTERS, 1997, 409 (01) :57-62
[10]   EPITOPE MAPPING OF MONOCLONAL-ANTIBODIES TO THE PAIRED HELICAL FILAMENTS OF ALZHEIMERS-DISEASE - IDENTIFICATION OF PHOSPHORYLATION SITES IN TAU-PROTEIN [J].
GOEDERT, M ;
JAKES, R ;
CROWTHER, RA ;
COHEN, P ;
VANMECHELEN, E ;
VANDERMEEREN, M ;
CRAS, P .
BIOCHEMICAL JOURNAL, 1994, 301 :871-877