The bright side of JNKs - Multitalented mediators in neuronal sprouting, brain development and nerve fiber regeneration

被引:110
作者
Waetzig, Vicki [1 ]
Zhao, Yi [1 ]
Herdegen, Thomas [1 ]
机构
[1] Univ Hosp Schleswig Holstein, Inst Pharmacol, D-24105 Kiel, Germany
关键词
axotomy; c-Jun; brain; development; injury; migration; neuritogenesis; neuron; sprouting;
D O I
10.1016/j.pneurobio.2006.08.002
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The c-Jun N-terminal kinases (JNKs) are important regulators of physiological and pathological processes in the central and peripheral nervous system. In general, JNKs are considered as mediators of neuronal degeneration in response to stress and injury. However, recent data have provided substantial evidence that JNKs are also essential for physiological and regenerative signalling in neurons. This review summarizes the importance of JNKs for neurite formation and outgrowth, brain development, dendritic architecture and regeneration of nerve fibers after injury. We discuss putative mechanisms which control the bipartite actions of individual JNK isoforms for neuronal death and repair after nerve fiber injury with a particular focus on the role of the transcription factor c-Jun. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:84 / 97
页数:14
相关论文
共 154 条
[71]   Up-regulation of Bak and Bim via JNK downstream pathway in the response to nitric oxide in human glioblastoma cells [J].
Jin, HO ;
Park, IC ;
An, S ;
Lee, HC ;
Woo, SH ;
Hong, YJ ;
Lee, SJ ;
Park, MJ ;
Yoo, DH ;
Rhee, CH ;
Hong, SI .
JOURNAL OF CELLULAR PHYSIOLOGY, 2006, 206 (02) :477-486
[72]   c-jun Can recruit JNK to phosphorylate dimerization partners via specific docking interactions [J].
Kallunki, T ;
Deng, TL ;
Hibi, M ;
Karin, M .
CELL, 1996, 87 (05) :929-939
[73]   JNK2 CONTAINS A SPECIFICITY-DETERMINING REGION RESPONSIBLE FOR EFFICIENT C-JUN BINDING AND PHOSPHORYLATION [J].
KALLUNKI, T ;
SU, B ;
TSIGELNY, I ;
SLUSS, HK ;
DERIJARD, B ;
MOORE, G ;
DAVIS, R ;
KARIN, M .
GENES & DEVELOPMENT, 1994, 8 (24) :2996-3007
[74]   DNA damaging agents induce expression of Fas ligand and subsequent apoptosis in T lymphocytes via the activation of NF-KB and AP-1 [J].
Kasibhatla, S ;
Brunner, T ;
Genestier, L ;
Echeverri, F ;
Mahboubi, A ;
Green, DR .
MOLECULAR CELL, 1998, 1 (04) :543-551
[75]   The in vivo roles of STEF/Tiam1, Rac1 and JNK in cortical neuronal migration [J].
Kawauchi, T ;
Chihama, K ;
Nabeshima, Y ;
Hoshino, M .
EMBO JOURNAL, 2003, 22 (16) :4190-4201
[76]   Morphogenesis of the telencephalic commissure requires scaffold protein JNK-interacting protein 3 (JIP3) [J].
Kelkar, N ;
Delmotte, MH ;
Weston, CR ;
Barrett, T ;
Sheppard, BJ ;
Flavell, RA ;
Davis, RJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (17) :9843-9848
[77]   Interaction of a mitogen-activated protein kinase signaling module with the neuronal protein JIP3 [J].
Kelkar, N ;
Gupta, S ;
Dickens, M ;
Davis, RJ .
MOLECULAR AND CELLULAR BIOLOGY, 2000, 20 (03) :1030-1043
[78]  
Kenney AM, 1998, J NEUROSCI, V18, P1318
[79]   c-Jun N-terminal kinase 3 deficiency protects neurons from axotomy-induced death in vivo through mechanisms independent of c-Jun phosphorylation [J].
Keramaris, E ;
Vanderluit, JL ;
Bahadori, M ;
Mousavi, K ;
Davis, RJ ;
Flavell, R ;
Slack, RS ;
Park, DS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (02) :1132-1141
[80]  
Kita Y, 1998, J CELL SCI, V111, P907