Author:
Whitmarsh Alan J.,Kuan Chia-Yi,Kennedy Norman J.,Kelkar Nyaya,Haydar Tarik F.,Mordes John P.,Appel Michael,Rossini Aldo A.,Jones Stephen N.,Flavell Richard A.,Rakic Pasko,Davis Roger J.
Abstract
The c-Jun N-terminal kinase (JNK) signal transduction pathway is activated in response to the exposure of cells to environmental stress. Components of the JNK signaling pathway interact with the JIP1 scaffold protein. JIP1 is located in the neurites of primary hippocampal neurons. However, in response to stress, JIP1 accumulates in the soma together with activated JNK and phosphorylated c-Jun. Disruption of theJip1 gene in mice by homologous recombination prevented JNK activation caused by exposure to excitotoxic stress and anoxic stress in vivo and in vitro. These data show that the JIP1 scaffold protein is a critical component of a MAP-kinase signal transduction pathway.
Publisher
Cold Spring Harbor Laboratory
Subject
Developmental Biology,Genetics
Cited by
212 articles.
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