Department of Medical and Molecular Genetics, King's College London, Guy's Medical School Campus, London, United Kingdom.
Cancer Res. 2010 May 15;70(10):3861-3. doi: 10.1158/0008-5472.CAN-10-0468. Epub 2010 Apr 20.
In mammalian cells the accumulation of repair proteins to double-strand breaks is a phosphorylation- and ubiquitylation-regulated process. Some of the genes that encode the kinases and ubiquitin ligases in this pathway are cancer predisposition genes, most prominently the breast cancer predisposition gene BRCA1, which encodes a ubiquitin ligase. How BRCA1 ligase activity was regulated following DNA damage was poorly understood. In this review I summarize new data that show a third post-translational modification, by the small ubiquitin like modifier SUMO, is part of the same cascade, enabling and activating DNA damage-regulated processes, including the BRCA1 ligase activity.
在哺乳动物细胞中，修复蛋白在双链断裂处的积累是一个磷酸化和泛素化调节的过程。该途径中的一些基因编码激酶和泛素连接酶，其中最突出的是乳腺癌易感基因 BRCA1，它编码一种泛素连接酶。BRCA1 连接酶活性在 DNA 损伤后是如何被调节的还不太清楚。在这篇综述中，我总结了一些新的数据，表明第三个翻译后修饰，即小泛素样修饰物 SUMO 的修饰，是同一级联反应的一部分，使包括 BRCA1 连接酶活性在内的 DNA 损伤调节过程得以进行和激活。
