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...

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Detalles Bibliográficos
Autores principales: Shao, Zhengping, Lee, Brian J, Rouleau-Turcotte, Élise, Langelier, Marie-France, Lin, Xiaohui, Estes, Verna M, Pascal, John M, Zha, Shan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2020
Materias:
Genome Integrity, Repair and Replication
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

Internet

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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