Ontology highlight
ABSTRACT: Background
Efficient and correct repair of DNA damage, especially DNA double-strand breaks, is critical for cellular survival. Defects in the DNA repair may lead to cell death or genomic instability and development of cancer. Non-homologous end-joining (NHEJ) is the major repair pathway for DNA double-strand breaks in mammalian cells. The ability of other repair pathways, such as homologous recombination, to compensate for loss of NHEJ and the ways in which contributions of different pathways are regulated are far from fully understood.Results
In this report we demonstrate that long single-stranded DNA (ssDNA) ends are formed at radiation-induced DNA double-strand breaks in NHEJ deficient cells. At repair times > or = 1 h, processing of unrejoined DNA double-strand breaks g
SUBMITTER: Karlsson KH
PROVIDER: S-EPMC2174948 | biostudies-literature | 2007 Oct
REPOSITORIES: biostudies-literature