ATF6 支持肿瘤细胞中的溶酶体功能，以实现 ER 应激激活的大自噬和 CMA：对突变 TP53 表达的影响

IF 14.6 1区生物学 Q1 CELL BIOLOGY

Autophagy Pub Date : 2024-04-02 DOI:10.1080/15548627.2024.2338577

Rossella Benedetti, Maria Anele Romeo, Andrea Arena, Maria Saveria Gilardini Montani, Gabriella D’Orazi, Mara Cirone

引用次数: 0

摘要

未折叠蛋白反应（UPR）通常能保护癌细胞免受应激，抑制UPR可增强诱导ER应激的药物的细胞毒性作用。然而，在...

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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ATF6 supports lysosomal function in tumor cells to enable ER stress-activated macroautophagy and CMA: impact on mutant TP53 expression

The inhibition of the unfolded protein response (UPR), which usually protects cancer cells from stress, may be exploited to potentiate the cytotoxic effect of drugs inducing ER stress. However, in ...

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来源期刊

Autophagy 生物-细胞生物学

CiteScore

21.30

自引率

2.30%

发文量

277

审稿时长

1 months

期刊介绍： Autophagy is a peer-reviewed journal that publishes research on autophagic processes, including the lysosome/vacuole dependent degradation of intracellular material. It aims to be the premier journal in the field and covers various connections between autophagy and human health and disease, such as cancer, neurodegeneration, aging, diabetes, myopathies, and heart disease. Autophagy is interested in all experimental systems, from yeast to human. Suggestions for specialized topics are welcome. The journal accepts the following types of articles: Original research, Reviews, Technical papers, Brief Reports, Addenda, Letters to the Editor, Commentaries and Views, and Articles on science and art. Autophagy is abstracted/indexed in Adis International Ltd (Reactions Weekly), EBSCOhost (Biological Abstracts), Elsevier BV (EMBASE and Scopus), PubMed, Biological Abstracts, Science Citation Index Expanded, Web of Science, and MEDLINE.