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...

詳細記述

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書誌詳細
出版年:Mol Cell
主要な著者: Dungrawala, Huzefa, Bhat, Kamakoti P., Le Meur, Rémy, Chazin, Walter J., Ding, Xia, Sharan, Shyam K., Wessel, Sarah R., Sathe, Aditya A., Zhao, Runxiang, Cortez, David
フォーマット: Artigo
言語:Inglês
出版事項: 2017
主題:
Article
オンライン･アクセス: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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