{"title":"53BP1-mediated activation of the tumor suppressor p53","authors":"","doi":"10.1016/j.ceb.2024.102424","DOIUrl":null,"url":null,"abstract":"<div><p>In recent years, the role of 53BP1 as a cell cycle regulator has come into the spotlight. 53BP1 is best understood for its role in controlling DNA double-strand break repair. However, 53BP1 was initially discovered as an interaction partner of the tumor suppressor p53, which proved to be independent of DNA repair. The importance of this interaction is becoming increasingly clear. 53BP1 responds to mitotic stress, which prolongs mitosis, or to DNA damage and triggers the stabilization of p53 by the deubiquitinase USP28 to stop the proliferation of potentially damaged cells. The ability of 53BP1 to respond to mitotic stress or DNA damage is controlled by cell cycle-specific post-translational modifications and is therefore restricted to specific cell cycle phases. 53BP1-mediated p53 activation is likely involved in tumor suppression and is associated with genetic diseases such as primary microcephaly. This review emphasizes the importance of these mechanisms for the development and maintenance of healthy tissues.</p></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":null,"pages":null},"PeriodicalIF":6.0000,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955067424001030/pdfft?md5=af2cd5b3e2fe21d2c6052021ec8030d5&pid=1-s2.0-S0955067424001030-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Opinion in Cell Biology","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0955067424001030","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
In recent years, the role of 53BP1 as a cell cycle regulator has come into the spotlight. 53BP1 is best understood for its role in controlling DNA double-strand break repair. However, 53BP1 was initially discovered as an interaction partner of the tumor suppressor p53, which proved to be independent of DNA repair. The importance of this interaction is becoming increasingly clear. 53BP1 responds to mitotic stress, which prolongs mitosis, or to DNA damage and triggers the stabilization of p53 by the deubiquitinase USP28 to stop the proliferation of potentially damaged cells. The ability of 53BP1 to respond to mitotic stress or DNA damage is controlled by cell cycle-specific post-translational modifications and is therefore restricted to specific cell cycle phases. 53BP1-mediated p53 activation is likely involved in tumor suppression and is associated with genetic diseases such as primary microcephaly. This review emphasizes the importance of these mechanisms for the development and maintenance of healthy tissues.
期刊介绍:
Current Opinion in Cell Biology (COCEBI) is a highly respected journal that specializes in publishing authoritative, comprehensive, and systematic reviews in the field of cell biology. The journal's primary aim is to provide a clear and readable synthesis of the latest advances in cell biology, helping specialists stay current with the rapidly evolving field. Expert authors contribute to the journal by annotating and highlighting the most significant papers from the extensive body of research published annually, offering valuable insights and saving time for readers by distilling key findings.
COCEBI is part of the Current Opinion and Research (CO+RE) suite of journals, which leverages the legacy of editorial excellence, high impact, and global reach to ensure that the journal is a widely read resource integral to scientists' workflow. It is published by Elsevier, a publisher known for its commitment to excellence in scientific publishing and the communication of reproducible biomedical research aimed at improving human health. The journal's content is designed to be an invaluable resource for a diverse audience, including researchers, lecturers, teachers, professionals, policymakers, and students.