RAD18 lives a double life: Its implication in DNA double-strand break repair

时间:2010年12月10日 访问次数:1536

DNA Repair (Amst). 2010 Dec 10;9(12):1241-8.

Ting Liu, Jun Huang*, Junjie Chen*

Abstract

Maintenance of genome stability depends on efficient and accurate repair of DNA lesions. Failure to prop- erly repair damaged DNA can cause cell death, mutations and chromosomal instability, which eventually lead to tumorigenesis. The E3 ligase RAD18 is well-knownfor its function in DNA damage by pass 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.

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