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首页> 外文期刊>Nucleus >Oxydative stress alters nuclear shape through lamins dysregulation: a route to senescence.
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Oxydative stress alters nuclear shape through lamins dysregulation: a route to senescence.

机译:氧化应激通过lamins失调来改变核的形状:这是衰老的途径。

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摘要

Progeroid phenotypes are mainly encountered in 2 types of syndromes: in laminopathies, which are characterized by nuclear shape abnormalities due to lamin A alteration, and in DNA damage response defect syndromes. Because lamin A dysregulation leads to DNA damages, it has been proposed that senescence occurs in both types of syndromes through the accumulation of damages. We recently showed that elevated oxidative stress is responsible for lamin B1 accumulation, nuclear shape alteration and senescence in the DDR syndrome, ataxia telangiectasia (A-T). Interestingly, overexpression of lamin B1 in wild type cells is sufficient to induce senescence without the induction of DNA damages. Here, we will discuss the importance of controlling the lamins level in order for maintenance nuclear architecture and we will comment the relationships of lamins with other senescence mechanisms. Finally, we will describe emerging data reporting redox control by lamins, leading us to propose a general mechanism by which reactive oxygen species can induce senescence through lamin dysregulation and NSA.
机译:早衰表型主要在两种类型的综合症中遇到:在椎间盘病变中,其特征是由于核纤层蛋白A改变引起的核形状异常;在DNA损伤反应缺陷综合症中。因为核纤层蛋白A失调导致DNA损伤,所以有人提出通过损伤的积累在两种类型的综合征中都发生衰老。我们最近发现,氧化应激升高是导致DDR综合征共济失调毛细血管扩张症(A-T)中lamin B1积累,核形状改变和衰老的原因。有趣的是,lamin B1在野生型细胞中的过表达足以诱导衰老,而不会引起DNA损伤。在这里,我们将讨论控制核纤层蛋白水平以维持核结构的重要性,并将评论核纤层蛋白与其他衰老机制的关系。最后,我们将描述新兴数据,这些数据报告了lamin对氧化还原的控制作用,从而使我们提出了一种通用的机制,通过该机制,活性氧可以通过lamin失调和NSA诱导衰老。

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