期刊
TRENDS IN GENETICS
卷 35, 期 11, 页码 783-785出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tig.2019.08.008
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资金
- NCI NIH HHS [R01 CA201446] Funding Source: Medline
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.
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