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

Liu Ting, Huang Jun, Chen Junjie

Research output: Contribution to journalReview articlepeer-review

29 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1241-1248
Number of pages8
JournalDNA Repair
Volume9
Issue number12
DOIs
StatePublished - Dec 10 2010

Keywords

  • Checkpoint
  • Homologous recombination (HR)
  • Post-replication repair (PRR)
  • RAD18

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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