4.7 Article

Cellular Stress Induces Nucleocytoplasmic Transport Deficits Independent of Stress Granules

期刊

BIOMEDICINES
卷 10, 期 5, 页码 -

出版社

MDPI
DOI: 10.3390/biomedicines10051057

关键词

neurodegeneration; amyotrophic lateral sclerosis; nuclear import; arsenite

资金

  1. VIB, KU Leuven
  2. Fund for Scientific Research Flanders (FWO-Vlaanderen)
  3. Agency for Innovation by Science and Technology (IWT
  4. SBO-iPSCAF)
  5. Thierry Latran Foundation
  6. 'Association Belge contre les Maladies neuro-Musculaires' (ABMM)
  7. ALS Liga Belgie (A Cure for ALS)
  8. FWO-Vlaanderen
  9. EMBO Long Term Fellowship
  10. E. von Behring Chair for Neuromuscular and Neurodegenerative Disorders
  11. KU Leuven fund Een Hart voor ALS
  12. KU Leuven fund Laeversfonds voor ALS Onderzoek
  13. KU Leuven fund Valery Perrier Race against ALS Fund

向作者/读者索取更多资源

The study aimed to investigate the causal relationship between stress granule formation and nucleocytoplasmic transport deficits. The results demonstrate that while stress granules are formed in response to cellular stress, they are not a direct cause of stress-induced nucleocytoplasmic transport deficits.
Stress granules are non-membrane bound granules temporarily forming in the cytoplasm in response to stress. Proteins of the nucleocytoplasmic transport machinery were found in these stress granules and it was suggested that stress granules contribute to the nucleocytoplasmic transport defects in several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS). The aim of this study was to investigate whether there is a causal link between stress granule formation and nucleocytoplasmic transport deficits. Therefore, we uncoupled stress granule formation from cellular stress while studying nuclear import. This was carried out by preventing cells from assembling stress granules despite being subjected to cellular stress either by knocking down both G3BP1 and G3BP2 or by pharmacologically inhibiting stress granule formation. Conversely, we induced stress granules by overexpressing G3BP1 in the absence of cellular stress. In both conditions, nuclear import was not affected demonstrating that stress granule formation is not a direct cause of stress-induced nucleocytoplasmic transport deficits.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据