Hutten Saskia, Wälde Sarah, Spillner Christiane, Hauber Joachim, Kehlenbach Ralph H
Department of Biochemistry I, Faculty of Medicine, Georg-August-University of Göttingen, 37073, Göttingen, Germany.
J Cell Sci. 2009 Apr 15;122(Pt 8):1100-10. doi: 10.1242/jcs.040154. Epub 2009 Mar 19.
Nup358 (also known as RanBP2), a component of the cytoplasmic filaments of the nuclear pore complex, has been implicated in various nucleocytoplasmic transport pathways. Here, we identify Nup358 as an important factor for transportin-mediated nuclear import. Depletion of Nup358 resulted in a strong inhibition of nuclear import of the human immunodeficiency virus type 1 (HIV-1) Rev protein. HIV-1 Rev is an RNA-binding protein that is required for CRM1 (also known as exportin 1)-dependent nuclear export of unspliced or partially spliced viral RNA. We show that transportin is the major nuclear import receptor for HIV-1 Rev in HeLa cells. Overexpression of transportin strongly promoted nuclear import of HIV-1 Rev in Nup358-depleted cells, indicating that the import receptor becomes rate-limiting under these conditions. Importantly, the import rate of other transportin-dependent proteins was also significantly reduced in Nup358-depleted cells. Our data therefore suggest a general role for Nup358 in transportin-mediated nuclear import.
核孔复合体胞质丝的组成成分Nup358（也称为RanBP2），已被证明参与多种核质运输途径。在此，我们确定Nup358是运输蛋白介导的核输入的一个重要因素。Nup358的缺失导致人类免疫缺陷病毒1型（HIV-1）Rev蛋白的核输入受到强烈抑制。HIV-1 Rev是一种RNA结合蛋白，对于未剪接或部分剪接的病毒RNA依赖CRM1（也称为输出蛋白1）的核输出是必需的。我们表明，在HeLa细胞中，运输蛋白是HIV-1 Rev的主要核输入受体。运输蛋白的过表达强烈促进了Nup358缺失细胞中HIV-1 Rev的核输入，这表明在这些条件下输入受体成为限速因素。重要的是，在Nup358缺失的细胞中，其他依赖运输蛋白的蛋白质的输入速率也显著降低。因此，我们的数据表明Nup358在运输蛋白介导的核输入中具有普遍作用。
