Surviving Telomere Attrition with the MiDAS Touch.

Flynn, Rachel L; Heaphy, Christopher M

Flynn, Rachel L; Heaphy, Christopher M.

Afiliação

Flynn RL; 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.
Heaphy CM; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: cheaphy@jhmi.edu.

Trends Genet ; 35(11): 783-785, 2019 11.

Article em En | MEDLINE | ID: mdl-31526614

ABSTRACT

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.

Assuntos

Telomerase/genética; Telômero; DNA; Replicação do DNA; Homeostase do Telômero; Tato

Palavras-chave

BLM; RAD52; SUMO; alternative lengthening of telomeres; mitotic DNA synthesis

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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Telômero / Telomerase Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2019 Tipo de documento: Article

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