RAD18 依赖的锌指结构域通过与泛素结合招募 SNM1A 至 DNA 修复复合物。
RAD18-dependent recruitment of SNM1A to DNA repair complexes by a ubiquitin-binding zinc finger.
机构信息
Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
出版信息
J Biol Chem. 2010 Jun 18;285(25):19085-91. doi: 10.1074/jbc.M109.100032. Epub 2010 Apr 12.
Abstract
SNM1A is a member of the SNM1 family of nucleases required for cellular processing of interstrand DNA crosslinks (ICLs). Little is known about the molecular function of SNM1A, in terms of its recruitment to ICL lesions or its DNA damage processing activity. Here we show that SNM1A contains a functional PIP box (PCNA-interacting protein box) and a UBZ (ubiquitin binding zinc finger), required for assembly of SNM1A into nuclear focus. Moreover, RAD18-dependent monoubiquitination of PCNA is required for Mitomycin C and Ultraviolet Light inducible SNM1A nuclear focus assembly. Taken together, our results identify a novel RAD18-PCNA(Ub)-SNM1A pathway required for nuclear focus formation and ICL resistance.
摘要
SNM1A 是 SNM1 家族的成员之一，该家族的核酸内切酶对于细胞内的链间 DNA 交联（ICLs）的处理是必需的。SNM1A 的分子功能，包括其对 ICL 损伤的募集或其 DNA 损伤处理活性，知之甚少。在这里，我们表明 SNM1A 含有一个功能性的 PIP 盒（PCNA 相互作用蛋白盒）和一个 UBZ（泛素结合锌指），这对于 SNM1A 组装成核焦点是必需的。此外，RAD18 依赖性的 PCNA 单泛素化对于丝裂霉素 C 和紫外线诱导的 SNM1A 核焦点组装是必需的。总之，我们的结果确定了一个新的 RAD18-PCNA（Ub）-SNM1A 途径，该途径对于核焦点的形成和 ICL 抗性是必需的。
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