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Clinical PARP inhibitors do not abrogate PARP1 exchange at DNA damage sites in vivo
DNA breaks recruit and activate PARP1/2, which deposit poly-ADP-ribose (PAR) to recruit XRCC1-Ligase3 and other repair factors to promote DNA repair. Clinical PARP inhibitors (PARPi) extend the lifetime of damage-induced PARP1/2 foci, referred to as ‘trapping’. To understand the molecular nature of...
Autores principales: | Shao, Zhengping, Lee, Brian J, Rouleau-Turcotte, Élise, Langelier, Marie-France, Lin, Xiaohui, Estes, Verna M, Pascal, John M, Zha, Shan |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7515702/ https://www.ncbi.nlm.nih.gov/pubmed/32890402 http://dx.doi.org/10.1093/nar/gkaa718 |
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