A cytoplasmic inhibitor of the JNK signal transduction pathway
A cytoplasmic inhibitor of the JNK signal transduction pathway
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DOI：
10.1126/science.277.5326.693
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发表时间：
1997-08-01
期刊：
影响因子：
56.9
通讯作者：
Davis, RJ
中科院分区：
文献类型：
--
作者：
Dickens, M;Rogers, JS;Davis, RJ
c-Jun氨基末端激酶（JNK）是涉及细胞生长控制的促分裂原活化蛋白（MAP）激酶的应激活化组的成员。一种特异性结合JNK的鼠细胞质蛋白[JNK相互作用蛋白-1（JIP-1）]被表征并克隆。JIP-1引起JNK的胞质滞留和JNK调节基因表达的抑制。此外，JIP-1抑制JNK信号通路对细胞增殖的影响，包括Bcr-Abl癌基因的转化。该分析将JIP-1鉴定为JNK信号转导通路的特异性抑制剂，并将蛋白质靶向确立为通过应激激活的MAP激酶调节信号传导的机制。
The c-Jun amino-terminal kinase (JNK) is a member of the stress-activated group of mitogen-activated protein (MAP) kinases that are implicated in the control of cell growth. A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned. JIP-1 caused cytoplasmic retention of JNK and inhibition of JNK-regulated gene expression. In addition, JIP-1 suppressed the effects of the JNK signaling pathway on cellular proliferation, including transformation by the Bcr-Abl oncogene. This analysis identifies JIP-1 as a specific inhibitor of the JNK signal transduction pathway and establishes protein targeting as a mechanism that regulates signaling by stress-activated MAP kinases.