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Surviving Telomere Attrition with the MiDAS Touch.
Trends in Genetics ( IF 11.4 ) Pub Date : 2019-09-13 , DOI: 10.1016/j.tig.2019.08.008
Rachel L Flynn 1 , Christopher M Heaphy 2
Affiliation  

Cancer cells maintain telomere lengths through telomerase activity or by alternative lengthening of telomeres (ALT). Using an engineered model system, a recent study by Min et al. reveals that the combination of BLM-mediated DNA resection and telomere clustering, a characteristic of ALT telomeres, catalyzes RAD52-dependent mitotic DNA synthesis (MiDAS) specifically at telomeres to drive ALT activity.

中文翻译:

使用MiDAS Touch挽救端粒磨损。

癌细胞通过端粒酶活性或端粒(ALT)的延长来维持端粒的长度。Min等人的最新研究使用工程模型系统。揭示了BLM介导的DNA切除和端粒簇聚(ALT端粒的特征)的结合,特别是在端粒上催化RAD52依赖的有丝分裂DNA合成(MiDAS),以驱动ALT活性。
更新日期:2019-09-13
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