Ran-independent nuclear import of cyclin B1-Cdc2 by importin β
Ran-independent nuclear import of cyclin B1-Cdc2 by importin β
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DOI：
10.1073/pnas.96.14.7938
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发表时间：
1999-07-06
影响因子：
11.1
通讯作者：
Morgan, DO
中科院分区：
文献类型：
--
作者：
Takizawa, CG;Weis, K;Morgan, DO
脊椎动物细胞中的有丝分裂由细胞周期蛋白 B1-Cdc2 复合物触发。该复合物在 G(2) 期末期的激活伴随着其从细胞质易位至细胞核。我们使用毛地黄皂苷透化的人类细胞来分析细胞周期蛋白 B1-Cdc2 导入细胞核的机制。细胞周期蛋白 B1-Cdc2 输入不会被输入蛋白 α 依赖性输入途径的抑制剂或 GTPase Ran 或输入蛋白 β 的显性失活版本阻断。然而，细胞周期蛋白 B1 的输入速率因细胞质中输入蛋白 β 的免疫耗竭而降低。在没有胞质或 Ran 且存在显性失活 Ran 突变体的情况下，纯化的 importin beta 促进了细胞周期蛋白 B1 的导入。我们得出的结论是，细胞周期蛋白 B1 输入是由一种不寻常的输入蛋白 β 依赖性机制介导的，该机制不需要 Ran。
Mitosis is triggered in vertebrate cells by the cyclin B1-Cdc2 complex. The activation of this complex at the end of G(2) phase is accompanied by its translocation from the cytoplasm to the nucleus. We used digitonin-permeabilized human cells to analyze the mechanism by which cyclin B1-Cdc2 is imported into the nucleus. Cyclin B1-Cdc2 import was not blocked by inhibitors of the importin alpha-dependent import pathway or by dominant negative versions of the GTPase Ran or importin beta. However, the rate of cyclin B1 import was decreased by immunodepletion of importin beta from cytosol. Purified importin beta promoted cyclin B1 import in the absence of cytosol or Ran and in the presence of the dominant negative Ran mutant. We conclude that cyclin B1 import is mediated by an unusual importin beta-dependent mechanism that does not require Ran.