010年10月22日在DNA Repair杂志在线发表综述文章“RAD18 lives a double life: its implication in DNA double-strand break repair”。其中刘婷博士为第一作者，黄俊博士与M.D.Anderson Cancer Center的Dr.Junjie Chen为共同通讯作者。

泛素E3连接酶RAD18在真核生物中十分保守，长期以来，RAD18在DNA损伤的复制后修复中的重要作用备受研究者关注。如果受到损伤的DNA在真核细胞进入DNA合成的S 期之前还未得到修复，细胞将会启动DNA损伤耐受机制（DTT,DNA damage tolerance）以顺利完成DNA复制。PCNA泛素化是DTT过程中的关键步骤，被单泛素化后的PCNA进而招募一系列非特异性DNA合成酶到DNA损伤位点，从而完成在DNA损伤存在条件下的DNA合成。而研究者们发现，对PCNA的泛素化主要是通过RAD18-RAD6这一E3-E2复合物完成。

除了复制后修复，很多研究表明RAD18可能在同源重组修复过程中也行使重要作用。在DNA双链损伤后，RNF8/UBC13泛素化H2A/H2AX，RAD18通过与H2A/H2AX的泛素化链相结合被招募到损伤位点，进而通过招募RAD51C参与DNA修复。这一过程不止在DNA同源重组修复中起重要作用，还作为DNA修复以及DNA检验点启动之间的平衡调节过程而在DNA损伤修复中行使重要功能。

本综述详尽阐述了RAD18蛋白在DNA损伤的复制后修复以及同源重组修复中的重要功能和作用机制

RAD18 livesadoublelife:ItsimplicationinDNAdouble-strandbreakrepair
Ting L, Jun H, Junjie C.

Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China.

Maintenance of genome stability depends on efficient and accurate repair of DNA lesions. Failure to properly repair damaged DNA can cause cell death, mutations and chromosomal instability, which eventually lead to tumorigenesis. The E3 ligase RAD18 is well-known for its function in DNA damage bypass and post-replication repair (PRR) in yeast and vertebrates via its ability to facilitate PCNA mono-ubiquitination at stalled replication forks. However, emerging evidence has also indicated that RAD18 plays an important role in homologous recombination (HR) in mammalian cells, which is an error-free DNA repair pathway that mediates the repair of double-strand breaks (DSBs). Here, we review how RAD18 carries out these distinct functions in response to different types of DNA lesions.