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翻译相关蛋白在p53调节中的作用:机制与意义

The Role of Translation-Associated Proteins in p53 Modulation: Mechanisms and Implications.

作者信息

Kałużyńska Daria

机构信息

Department of Systems Biology and Engineering, Silesian University of Technology, Akademicka 16, 44-100 Gliwice, Poland.

出版信息

Int J Mol Sci. 2025 Aug 22;26(17):8164. doi: 10.3390/ijms26178164.

DOI:10.3390/ijms26178164
PMID:40943089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12428463/
Abstract

Translation is the final stage of protein synthesis and involves a broad range of proteins-from those directly participating in the process, such as initiation factors and ribosomal components, to those involved in post-translational regulation. Beyond their canonical functions, many of these proteins also influence key signaling pathways, including those regulating cellular stress responses and tumor suppression. This review explores the current knowledge of translation-associated proteins that modulate the tumor-suppressor protein p53. It highlights the roles of ribosomal proteins, stress arising from impaired ribosome biogenesis (nucleolar stress), and various translation-related factors in influencing p53 stability and activity. By integrating findings from diverse studies, this work provides insight into the intricate interplay between translation and p53 signaling, emphasizing its relevance for cellular homeostasis and stress adaptation.

摘要

翻译是蛋白质合成的最后阶段,涉及多种蛋白质——从直接参与该过程的蛋白质,如起始因子和核糖体成分,到参与翻译后调控的蛋白质。除了其经典功能外,这些蛋白质中的许多还影响关键信号通路,包括调节细胞应激反应和肿瘤抑制的信号通路。本综述探讨了目前对调节肿瘤抑制蛋白p53的翻译相关蛋白质的认识。它强调了核糖体蛋白的作用、核糖体生物发生受损(核仁应激)产生的应激以及各种翻译相关因子在影响p53稳定性和活性方面的作用。通过整合来自不同研究的结果,这项工作深入了解了翻译与p53信号之间的复杂相互作用,强调了其对细胞稳态和应激适应的相关性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc2c/12428463/2aeb44625d91/ijms-26-08164-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc2c/12428463/7411462747b6/ijms-26-08164-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc2c/12428463/2cb7af5e59ab/ijms-26-08164-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc2c/12428463/2aeb44625d91/ijms-26-08164-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc2c/12428463/7411462747b6/ijms-26-08164-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc2c/12428463/2cb7af5e59ab/ijms-26-08164-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc2c/12428463/2aeb44625d91/ijms-26-08164-g003.jpg

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BMC Med Genomics. 2025 Apr 18;18(1):77. doi: 10.1186/s12920-025-02133-4.
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RPS15a knockdown impedes the progression of B-ALL by inducing p53-mediated nucleolar stress.核糖体蛋白S15a(RPS15a)敲低通过诱导p53介导的核仁应激来阻碍B淋巴细胞白血病(B-ALL)的进展。
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