{"title":"53BP1 介导的肿瘤抑制因子 p53 激活","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":"{\"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}","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
摘要
近年来,53BP1 作为细胞周期调控因子的作用成为人们关注的焦点。人们最了解 53BP1 在控制 DNA 双链断裂修复中的作用。然而,53BP1 最初是作为肿瘤抑制因子 p53 的相互作用伙伴被发现的,事实证明它与 DNA 修复无关。这种相互作用的重要性正变得越来越清楚。53BP1 可对有丝分裂压力或 DNA 损伤做出反应,从而延长有丝分裂时间,并通过去泛素化酶 USP28 触发 p53 的稳定,以阻止可能受损细胞的增殖。53BP1 对有丝分裂应激或 DNA 损伤的反应能力受细胞周期特异性翻译后修饰的控制,因此仅限于特定的细胞周期阶段。53BP1 介导的 p53 激活可能参与了肿瘤抑制,并与原发性小头畸形等遗传疾病有关。本综述强调了这些机制对健康组织的发育和维护的重要性。
53BP1-mediated activation of the tumor suppressor p53
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.