Requirement of the JIP1 scaffold protein for stress-induced JNK activation
Requirement of the JIP1 scaffold protein for stress-induced JNK activation
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DOI：
10.1101/gad.922801
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发表时间：
2001-09-15
影响因子：
10.5
通讯作者：
Davis, RJ
中科院分区：
文献类型：
--
作者：
Whitmarsh, AJ;Kuan, CY;Davis, RJ
c-Jun n -末端激酶（INK）信号转导通路在细胞暴露于环境应激时被激活。INK信号通路的组分与JIP1支架蛋白相互作用。JIP1位于海马初级神经元的神经突中。然而，在应激反应中，JIP1与活化的JNK和磷酸化的c-Jun一起在体细胞中积累。通过同源重组破坏小鼠的jip1基因，可以在体内和体外阻止暴露于兴奋毒性应激和缺氧应激引起的JNK激活。这些数据表明，JIP1支架蛋白是map -激酶信号转导途径的关键组成部分。
The c-Jun N-terminal kinase (INK) signal transduction pathway is activated in response to the exposure of cells to environmental stress. Components of the INK 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 the jip1 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.