核糖体组装失调时的 MDM4 外显子跳转。

IF 13 1区生物学 Q1 CELL BIOLOGY

Trends in Cell Biology Pub Date : 2024-11-07 DOI:10.1016/j.tcb.2024.10.006

Jennifer Jansen, Matthias Dobbelstein

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引用次数: 0

摘要

最近的研究揭示了核极应激如何通过核糖体蛋白 L22（RPL22；eL22）增强 MDM4 外显子跳越并激活 p53。肿瘤相关的 L22 突变会导致全长 MDM4 合成，从而克服 p53 对肿瘤的抑制。本论坛文章探讨了 MDM4 剪接模式如何整合应激信号，以作出依赖于 p53 的细胞命运决定。

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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MDM4 exon skipping upon dysfunctional ribosome assembly.

Recent studies revealed how nucleolar stress enhances MDM4 exon skipping and activates p53 via the ribosomal protein L22 (RPL22; eL22). Tumor-associated L22 mutations lead to full-length MDM4 synthesis, overcoming tumor suppression by p53. This forum article explores how MDM4 splicing patterns integrate stress signaling to take p53-dependent cell fate decisions.

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来源期刊

Trends in Cell Biology 生物-细胞生物学

CiteScore

32.00

自引率

0.50%

发文量

160

审稿时长

61 days

期刊介绍： Trends in Cell Biology stands as a prominent review journal in molecular and cell biology. Monthly review articles track the current breadth and depth of research in cell biology, reporting on emerging developments and integrating various methods, disciplines, and principles. Beyond Reviews, the journal features Opinion articles that follow trends, offer innovative ideas, and provide insights into the implications of new developments, suggesting future directions. All articles are commissioned from leading scientists and undergo rigorous peer-review to ensure balance and accuracy.