TDP2-dependent non-homologous end-joining protects against topoisomerase II-induced DNA breaks and genome instability in cells and in vivo.
Anticancer topoisomerase "poisons" exploit the break-and-rejoining mechanism of topoisomerase II (TOP2) to generate TOP2-linked DNA double-strand breaks (DSBs). This characteristic underlies the clinical efficacy of TOP2 poisons, but is also implicated in chromosomal translocations and gen...
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Auteurs principaux: | , , , , , , , , , , |
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Format: | article |
Langue: | EN |
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Public Library of Science (PLoS)
2013
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Accès en ligne: | https://doaj.org/article/b6ee006f88034a179df6e3efdebf08fa |
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