用 MiDAS 疗法维持端粒体损耗。

Surviving Telomere Attrition with the MiDAS Touch.

机构信息

Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA; Department of Medicine, Boston University School of Medicine, Boston, MA, USA; Cancer Center, Boston University School of Medicine, Boston, MA, USA.

Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

出版信息

Trends Genet. 2019 Nov;35(11):783-785. doi: 10.1016/j.tig.2019.08.008. Epub 2019 Sep 13.

DOI:10.1016/j.tig.2019.08.008

PMID:31526614

Abstract

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.

摘要

癌细胞通过端粒酶活性或通过端粒的非经典延长（ALT）来维持端粒长度。最近，Min 等人在一个工程模型系统中进行的一项研究表明，BLM 介导的 DNA 切除与端粒聚集（ALT 端粒的特征）的组合，可特异性地在端粒上催化 RAD52 依赖性有丝分裂 DNA 合成（MiDAS），从而驱动 ALT 活性。