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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Autores principales: Fernando Gómez-Herreros, Rocío Romero-Granados, Zhihong Zeng, Alejandro Alvarez-Quilón, Cristina Quintero, Limei Ju, Lieve Umans, Liesbeth Vermeire, Danny Huylebroeck, Keith W Caldecott, Felipe Cortés-Ledesma
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2013
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Acceso en línea:https://doaj.org/article/b6ee006f88034a179df6e3efdebf08fa
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