کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9881288 | 1535696 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Making ends meet in old age: DSB repair and aging
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Accumulation of somatic mutations has long been considered as a major cause of aging and age-related diseases such as cancer. Genomic rearrangements, which arise from aberrant repair of DNA breaks, are the most characteristic component of the mutation spectra in aging cells and tissues. The studies conducted in the past few years provide further support for the role of DNA double-strand break (DSB) repair in aging and cellular senescence. Evidence was obtained that in addition to accumulation of mutations the efficiency and fidelity of repair declines with age. We propose that DNA damage and age-related decline of DNA repair form a vicious cycle leading to amplification of damage and progression of aging, and discuss a hypothesis on how the interplay between the two pathways of DSB repair, homologous recombination and nonhomologous end joining, may contribute to the aging process.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mechanisms of Ageing and Development - Volume 126, Issues 6â7, JuneâJuly 2005, Pages 621-628
Journal: Mechanisms of Ageing and Development - Volume 126, Issues 6â7, JuneâJuly 2005, Pages 621-628
نویسندگان
Vera Gorbunova, Andrei Seluanov,