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RADX promotes genome stability and modulates chemosensitivity by regulating RAD51 at replication forks
RAD51 promotes homology-directed repair (HDR), replication fork reversal, and stalled fork protection. Defects in these functions cause genomic instability and tumorigenesis, but also generate hypersensitivity to cancer therapeutics. Here we describe the identification of RADX as an RPA-like, single...
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| Yayımlandı: | Mol Cell |
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| Asıl Yazarlar: | , , , , , , , , , |
| Materyal Türü: | Artigo |
| Dil: | Inglês |
| Baskı/Yayın Bilgisi: |
2017
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| Konular: | |
| Online Erişim: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5548441/ https://ncbi.nlm.nih.gov/pubmed/28735897 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.molcel.2017.06.023 |
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