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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...
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| 發表在: | Nucleic Acids Res |
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| Main Authors: | , , , , , , , |
| 格式: | Artigo |
| 語言: | Inglês |
| 出版: |
Oxford University Press
2020
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| 主題: | |
| 在線閱讀: | https://ncbi.nlm.nih.gov/pmc/articles/PMC7515702/ https://ncbi.nlm.nih.gov/pubmed/32890402 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/nar/gkaa718 |
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