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首页> 外文期刊>Molecular and Cellular Biology >Nup214 Is Required for CRM1-Dependent Nuclear Protein Export In Vivo
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Nup214 Is Required for CRM1-Dependent Nuclear Protein Export In Vivo

机译：依赖CRM1的体内核蛋白出口需要Nup214

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Nucleoporins mediate transport of macromolecules across the nuclear pore complex, yet the function of many individual nucleoporins is largely unresolved. To address this question, we depleted cells of the cytoplasmic nucleoporins Nup214/CAN and Nup358/RanBP2 by RNA interference. Depletion of Nup214 resulted in codepletion of its binding partner, Nup88. Nuclear pore complexes assembled in the absence of Nup214/Nup88 or Nup358 were fully functional in nuclear protein import, whereas nuclear mRNA export was slightly impaired. Depletion of Nup358 had only a minor effect on nuclear protein export. In contrast, depletion of Nup214/Nup88 led to strongly reduced CRM1-mediated export of the shuttling transcription factor NFAT as well as a human immunodeficiency virus-Rev derivative. A specific role of Nup214 in protein export is furthered by the biochemical properties of a high-affinity complex containing Nup214, CRM1, RanGTP, and an export cargo. Our results show that the Nup214/Nup88 complex is required for efficient CRM1-mediated transport, supporting a model involving a high-affinity binding site for CRM1 at Nup214 in the terminal steps of export.
机译：核蛋白素介导大分子跨核孔复合物的转运，但许多单个核孔蛋白的功能在很大程度上尚未得到解决。为了解决这个问题，我们通过RNA干扰消除了细胞质核孔蛋白Nup214 / CAN和Nup358 / RanBP2的细胞。 Nup214的耗竭导致其结合伴侣Nup88的代码耗竭。在没有Nup214 / Nup88或Nup358的情况下组装的核孔复合物在核蛋白的导入中具有全部功能，而核mRNA的输出则受到轻微损害。 Nup358的耗竭对核蛋白的出口影响很小。相反，Nup214 / Nup88的耗尽导致CRM1介导的穿梭转录因子NFAT以及人类免疫缺陷病毒-Rev衍生物的输出大大减少。 Nup214在蛋白质输出中的特定作用通过包含Nup214，CRM1，RanGTP和出口货物的高亲和力复合物的生化特性进一步增强。我们的结果表明，Nup214 / Nup88复合物是有效的CRM1介导运输所必需的，支持了在出口的最终步骤中涉及Nup214处CRM1高亲和力结合位点的模型。

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