压力下的 TUDOR 蛋白的失活揭示了染色质与 53BP1 之间的关联。
The demise of a TUDOR under stress opens a chromatin link to 53BP1.
机构信息
School of Cancer Sciences, University of Birmingham, Birmingham, UK.
出版信息
EMBO J. 2012 Apr 18;31(8):1847-9. doi: 10.1038/emboj.2012.78. Epub 2012 Mar 27.
Abstract
EMBO J (2012) 31 8, 1865–1878. doi:; DOI: 10.1038/emboj.2012.47 The mechanisms that localise 53BP1 to sites of DNA double-strand breaks (DSBs) have remained elusive, despite this protein’s key roles in DNA damage response signalling and repair processes. Recent studies, including the work by Mallette et al (2012) in this issue of , now provide crucial insights into the roles of ubiquitin-dependent signalling cascades at DNA damage sites required for chromatin-mediated 53BP1 recruitment.
摘要
EMBO J (2012) 31 8, 1865–1878. doi:; DOI: 10.1038/emboj.2012.47 尽管 53BP1 在 DNA 损伤反应信号转导和修复过程中起着关键作用，但将其定位到 DNA 双链断裂 (DSB) 位点的机制仍未被揭示。最近的研究，包括 Mallette 等人（2012）在本期 中的工作，现在为需要染色质介导的 53BP1 募集的 DNA 损伤位点上依赖泛素的信号级联反应在发挥作用提供了重要的见解。
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