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HIV-1 Vpr induces defects in mitosis, cytokinesis, nuclear structure, and centrosomes

机译:HIV-1 Vpr诱导有丝分裂,胞质分裂,核结构和中心体的缺陷

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Human immunodeficiency virus type 1 (HIV-1) Vpr is a 15-kDa accessory protein that contributes to several steps in the viral replication cycle and promotes virus-associated pathology. Previous studies demonstrated that Vpr inhibits G2/M cell cycle progression in both human cells and in the fission yeast Schizosaccharomyces pombe. Here, we report that, upon induction of vpr expression, fission yeast exhibited numerous defects in the assembly and function of the mitotic spindle. In particular, two spindle pole body proteins, sad1p and the polo kinase plo1p, were delocalized in vpr-expressing yeast cells, suggesting that spindle pole body integrity was perturbed. In addition, nuclear envelope structure, contractile actin ring formation, and cytokinesis were also disrupted. Similar Vpr-induced defects in mitosis and cytokinesis were observed in human cells, including aberrant mitotic spindles, multiple centrosomes, and multinucleate cells. These defects in cell division and centrosomes might account for some of the pathological effects associated with HIV-1 infection. [References: 53]
机译:人类1型免疫缺陷病毒(HIV-1)Vpr是一种15 kDa的辅助蛋白,可参与病毒复制周期的多个步骤并促进与病毒相关的病理。先前的研究表明,Vpr抑制人细胞和裂殖酵母粟酒裂殖酵母中的G2 / M细胞周期进程。在这里,我们报告说,在诱导vpr表达后,裂变酵母在有丝分裂纺锤体的组装和功能中表现出许多缺陷。特别是,两个纺锤极体蛋白,sad1p和polo激酶plo1p,在表达vpr的酵母细胞中被脱位,表明纺锤体的完整性受到干扰。此外,核被膜结构,收缩性肌动蛋白环形成和胞质分裂也被破坏。在人类细胞中观察到类似的Vpr诱导的有丝分裂和胞质分裂缺陷,包括异常的有丝分裂纺锤体,多个中心体和多核细胞。细胞分裂和中心体的这些缺陷可能是与HIV-1感染相关的某些病理影响的原因。 [参考:53]

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