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Ran的核输入由运输因子NTF2介导。

Nuclear import of Ran is mediated by the transport factor NTF2.

作者信息

Smith A, Brownawell A, Macara I G

机构信息

Center for Cell Signaling, Health Sciences Center, University of Virginia, Charlottesville, Virginia 22908, USA.

出版信息

Curr Biol. 1998;8(25):1403-6. doi: 10.1016/s0960-9822(98)00023-2.

Abstract

A concentration gradient of the GTP-bound form of the GTPase Ran across nuclear pores is essential for the transport of many proteins and nucleic acids between the nuclear and cytoplasmic compartments of eukaryotic cells [1] [2] [3] [4]. The mechanisms responsible for the dynamics and maintenance of this Ran gradient have been unclear. We now show that Ran shuttles between the nucleosol and cytosol, and that cytosolic Ran accumulates rapidly in the nucleus in a saturable manner that is dependent on temperature and on the guanine-nucleotide exchange factor RCC1. Nuclear import in digitonin-permeabilized cells in the absence of added factors was minimal. The addition of energy and nuclear transport factor 2 (NTF2) [5] was sufficient for the accumulation of Ran in the nucleus. An NTF2 mutant that cannot bind Ran [6] was unable to facilitate Ran import. A GTP-bound form of a Ran mutant that cannot bind NTF2 was not a substrate for import. A dominant-negative importin-beta mutant inhibited nuclear import of Ran, whereas addition of transportin, which accumulates in the nucleus, enhanced NTF2-dependent Ran import. We conclude that NTF2 functions as a transport receptor for Ran, permitting rapid entry into the nucleus where GTP-GDP exchange mediated by RCC1 [7] converts Ran into its GTP-bound state. The Ran-GTP can associate with nuclear Ran-binding proteins, thereby creating a Ran gradient across nuclear pores.

摘要

小GTP酶Ran的GTP结合形式在核孔间形成的浓度梯度,对于真核细胞的核质区室间多种蛋白质和核酸的运输至关重要[1][2][3][4]。负责这种Ran梯度动态变化和维持的机制尚不清楚。我们现在表明,Ran穿梭于核质和细胞质之间,并且细胞质中的Ran以一种依赖于温度和鸟嘌呤核苷酸交换因子RCC1的可饱和方式迅速在细胞核中积累。在没有添加因子的情况下,洋地黄皂苷通透细胞中的核输入极少。添加能量和核运输因子2(NTF2)[5]足以使Ran在细胞核中积累。一种不能结合Ran的NTF2突变体无法促进Ran的输入。一种不能结合NTF2的Ran突变体的GTP结合形式不是输入的底物。一种显性负性的输入蛋白β突变体抑制了Ran的核输入,而添加积累在细胞核中的运输蛋白则增强了NTF2依赖的Ran输入。我们得出结论,NTF2作为Ran的运输受体发挥作用,允许其快速进入细胞核,在那里由RCC1[7]介导的GTP-GDP交换将Ran转化为其GTP结合状态。Ran-GTP可与核Ran结合蛋白结合,从而在核孔间形成Ran梯度。

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