Central Radioisotope Division, National Cancer Center Research Institute, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
Genes (Basel). 2021 Nov 5;12(11):1763. doi: 10.3390/genes12111763.
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.
范可尼贫血（FA）DNA 修复途径协调了一种忠实的修复机制，用于修复因 DNA 链间交联（ICLs）或复制压力等因素而停滞的 DNA 复制叉。FA 途径激活的一个重要作用是由 FANCD2 和其结合伴侣 FANCI 的单泛素化起始的，这一过程受 ATM 相关激酶 ATR 调节。因此，FA 途径的调控是 ATR 对基因组稳定性贡献的一个很好的例子。在这篇简短的综述中，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泛素化激活的知识。
