短期热量限制促进小鼠非同源末端连接的DNA修复。

IF 5.4 Q1 GERIATRICS & GERONTOLOGY
NPJ Aging and Mechanisms of Disease Pub Date : 2020-08-14 eCollection Date: 2020-01-01 DOI:10.1038/s41514-020-00047-2
Zhonghe Ke, Denis Firsanov, Brianna Spencer, Andrei Seluanov, Vera Gorbunova
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引用次数: 11

摘要

热量限制(CR)可以改善包括老鼠在内的多种生物的健康,降低癌症发病率并延长寿命。CR可增强DNA修复的碱基切除修复和核苷酸切除修复途径,但CR是否能改善DNA双链断裂的修复尚未在体内系统中得到验证。在这里,我们利用非同源末端连接(NHEJ)报告小鼠来证明短期CR强烈增强NHEJ的DNA修复,这与DNA- pk和SIRT6水平升高有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Short-term calorie restriction enhances DNA repair by non-homologous end joining in mice.

Short-term calorie restriction enhances DNA repair by non-homologous end joining in mice.

Calorie restriction (CR) improves health, reduces cancer incidence and extends lifespan in multiple organisms including mice. CR was shown to enhance base excision repair and nucleotide excision repair pathways of DNA repair, however, whether CR improves repair of DNA double-strand breaks has not been examined in in vivo system. Here we utilize non-homologous end joining (NHEJ) reporter mice to show that short-term CR strongly enhances DNA repair by NHEJ, which is associated with elevated levels of DNA-PK and SIRT6.

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来源期刊
NPJ Aging and Mechanisms of Disease
NPJ Aging and Mechanisms of Disease Medicine-Geriatrics and Gerontology
自引率
0.00%
发文量
0
审稿时长
8 weeks
期刊介绍: npj Aging and Mechanisms of Disease is an online open access journal that provides a forum for the world’s most important research in the fields of aging and aging-related disease. The journal publishes papers from all relevant disciplines, encouraging those that shed light on the mechanisms behind aging and the associated diseases. The journal’s scope includes, but is not restricted to, the following areas (not listed in order of preference): • cellular and molecular mechanisms of aging and aging-related diseases • interventions to affect the process of aging and longevity • homeostatic regulation and aging • age-associated complications • translational research into prevention and treatment of aging-related diseases • mechanistic bases for epidemiological aspects of aging-related disease.
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