Regulation of the ubiquitin system by checkpoint kinases in response to stalled replication forks

面部贫血是一种遗传性疾病，其特征是进行性骨髓衰竭，癌症发病率增加，以及由泛素系统驱动的DNA修复不足。在这项研究中，我们阐明了检查点激酶ATR在触发DNA损伤诱导的FA DNA修复途径激活中的作用。此外，我们还发现一些FA蛋白促进必要的ATR相互作用蛋白与染色质的结合。

Faconi anemia(FA) is a hereditary disorder characterized by progressive bone marrow failure, increased incidence of cancer, and deficiency of DNA repair driven by the ubiquitin system. In this study, we have clarified a role of checkpoint kinase ATR in triggering DNA damage-induced activation of theFA DNA repair pathway. Furthermore, we have discovered that some FA proteins promote association of essential ATR interacter ATRIP to chromatin.