RAD18 lives a double life: Its implication in DNA double-strand break repair.
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.
Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Liu
L
Ting
Huang
H
Jun
Chen
C
Junjie
D053903:DNA Breaks, Double-Stranded; D004260:DNA Repair / Q000235:genetics / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D018816:Genes, cdc / Q000502:physiology; D042822:Genomic Instability / Q000235:genetics*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011995:Recombination, Genetic / Q000502:physiology*; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism*; D054875:Ubiquitination
D004268:DNA-Binding Proteins; D018809:Proliferating Cell Nuclear Antigen; C485954:RAD18 protein, human; D044767:Ubiquitin-Protein Ligases