PDF(Pubmed)
Abstract：
The Fanconi anemia (FA) DNA repair pathway coordinates a faithful repair mechanism for stalled DNA replication forks caused by factors such as DNA interstrand crosslinks (ICLs) or replication stress. An important role of FA pathway activation is initiated by monoubiquitination of FANCD2 and its binding partner of FANCI, which is regulated by the ATM-related kinase, ATR. Therefore, regulation of the FA pathway is a good example of the contribution of ATR to genome stability. In this short review, we summarize the knowledge accumulated over the years regarding how the FA pathway is activated via phosphorylation and monoubiquitination.
摘要：
范可尼贫血（FA）DNA修复途径协调了由DNA链间交联（ICL）或复制应激等因素引起的停滞DNA复制叉的忠实修复机制。FA途径激活的一个重要作用是由FANCD2及其FANCI的结合配偶体的单单泛素化启动，这是由ATM相关激酶调节的，ATR.因此,FA途径的调节是ATR对基因组稳定性的贡献的一个很好的例子。在这篇简短的评论中，我们总结了多年来积累的关于FA途径如何通过磷酸化和单尿素化激活的知识.
