NMDA介导的信号转导对JIP支架蛋白的需求。
Requirement of JIP scaffold proteins for NMDA-mediated signal transduction.
作者信息
Kennedy Norman J, Martin Gilles, Ehrhardt Anka G, Cavanagh-Kyros Julie, Kuan Chia-Yi, Rakic Pasko, Flavell Richard A, Treistman Steven N, Davis Roger J
机构信息
Howard Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
出版信息
Genes Dev. 2007 Sep 15;21(18):2336-46. doi: 10.1101/gad.1563107.
Abstract
JIP scaffold proteins are implicated in the regulation of protein kinase signal transduction pathways. To test the physiological role of these scaffold proteins, we examined the phenotype of compound mutant mice that lack expression of JIP proteins. These mice were found to exhibit severe defects in N-methyl-D-aspartic acid (NMDA) receptor function, including decreased NMDA-evoked current amplitude, cytoplasmic Ca(++), and gene expression. The decreased NMDA receptor activity in JIP-deficient neurons is associated with reduced tyrosine phosphorylation of NR2 subunits of the NMDA receptor. JIP complexes interact with the SH2 domain of cFyn and may therefore promote tyrosine phosphorylation and activity of the NMDA receptor. We conclude that JIP scaffold proteins are critically required for normal NMDA receptor function.
摘要
JIP支架蛋白参与蛋白激酶信号转导通路的调控。为了测试这些支架蛋白的生理作用，我们检测了缺乏JIP蛋白表达的复合突变小鼠的表型。发现这些小鼠在N-甲基-D-天冬氨酸（NMDA）受体功能方面表现出严重缺陷，包括NMDA诱发电流幅度降低、细胞质钙离子浓度降低以及基因表达减少。JIP缺陷神经元中NMDA受体活性降低与NMDA受体NR2亚基酪氨酸磷酸化减少有关。JIP复合物与cFyn的SH2结构域相互作用，因此可能促进NMDA受体的酪氨酸磷酸化和活性。我们得出结论，正常的NMDA受体功能严重需要JIP支架蛋白。
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