近年来，53BP1作为细胞周期调节剂的作用受到人们的关注。 53BP1 最被理解的是它在控制 DNA 双链断裂修复中的作用。然而，53BP1 最初被发现是肿瘤抑制因子 p53 的相互作用伴侣，并被证明与 DNA 修复无关。这种互动的重要性越来越明显。 53BP1 对有丝分裂应激作出反应，从而延长有丝分裂，或对 DNA 损伤做出反应，并通过去泛素酶 USP28 触发 p53 的稳定，以阻止可能受损的细胞的增殖。 53BP1 响应有丝分裂应激或 DNA 损伤的能力由细胞周期特异性翻译后修饰控制，因此仅限于特定的细胞周期阶段。 53BP1 介导的 p53 激活可能参与肿瘤抑制，并与原发性小头畸形等遗传性疾病相关。本综述强调了这些机制对于健康组织的发育和维护的重要性。版权所有 © 2024 作者。由爱思唯尔有限公司出版。保留所有权利。

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.Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.