CRM1 is an export receptor for leucine-rich nuclear export signals
CRM1 is an export receptor for leucine-rich nuclear export signals
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DOI：
10.1016/s0092-8674(00)80371-2
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发表时间：
1997-09-19
期刊：
影响因子：
64.5
通讯作者：
Mattaj, IW
中科院分区：
文献类型：
--
作者：
Fornerod, M;Ohno, M;Mattaj, IW
CRM1与介导核蛋白输入的受体有较远的亲缘关系，以前曾被证明与核孔复合体相互作用。在非洲爪哇卵母细胞中过表达CRM1可刺激Rev和U SnRNA从细胞核输出。相反，软霉素B，一种被证明与CRM1蛋白结合的细胞毒素，特异性地抑制REV和U SNRNAs的核输出。在体外，CRM1形成一个轻霉素B敏感的复合体，涉及RanGTP和来自REV或PKI蛋白的核输出信号(NES)的协同结合。我们得出结论，CRM1是富含亮氨酸的核输出信号的输出受体，并讨论了RanGTP在CRM1功能和一般核输出中的作用模型。
CRM1 is distantly related to receptors that mediate nuclear protein import and was previously shown to interact with the nuclear pore complex. Overexpression of CRM1 in Xenopus oocytes stimulates Rev and U snRNA export from the nucleus. Conversely, leptomycin B, a cytotoxin that is shown to bind to CRM1 protein, specifically inhibits the nuclear export of Rev and U snRNAs. In vitro, CRM1 forms a leptomycin B-sensitive complex involving cooperative binding of both RanGTP and the nuclear export signal (NES) from either the Rev or PKI proteins. We conclude that CRM1 is an export receptor for leucine-rich nuclear export signals and discuss a model for the role of RanGTP in CRM1 function and in nuclear export in general.