Non homologous end joining-mediated DNA break repair is impaired in B lymphocytes of aging mice

Puthiyaveetil, Abdul Gafoor; Caudell, David L.

doi:10.1016/j.molimm.2012.07.001

Cited by 2 publications

(3 citation statements)

References 59 publications

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“…It has been reported that age may diminish the effectiveness of the two main DSB repair pathways (NHEJ and HR). Using plasmid ligation methodologies, a recent study has shown that B lymphocytes from old mice show poor NHEJ repair efficiency and increased misrepair compared with younger mice (Puthiyaveetil & Caudell, 2013 ). Using a similar approach, Seluanov et al .…”

Section: Impaired Dna Repair Of the Aging Cellsmentioning

confidence: 99%

“…The same authors also observed that the levels of Ku―a key component of the NHEJ pathway responsible for keeping close together the two broken DNA ends―were diminished in senescent cells (Seluanov et al ., 2007 ). Reduced efficiency of NHEJ in the elderly might result in persistent DSBs leading to misrejoining events and genomic instability, and also in impaired V(D)J recombination, which could contribute to reduce the immune cell repository and thus the immune system (Puthiyaveetil & Caudell, 2013 ). As the immune system uses its diverse antigen receptor repertoire to prevent tumor formation and progression, NHEJ impairment could eventually lead to a carcinogenic prone scenario (Li et al ., 2011 ).…”

Section: Impaired Dna Repair Of the Aging Cellsmentioning

confidence: 99%

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Aging and radiation: bad companions

et al. 2015

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Aging involves a deterioration of cell functions and changes that may predispose the cell to undergo an oncogenic transformation. The carcinogenic risks following radiation exposure rise with age among adults. Increasing inflammatory response, loss of oxidant/antioxidant equilibrium, ongoing telomere attrition, decline in the DNA damage response efficiency, and deleterious nuclear organization are age-related cellular changes that trigger a serious threat to genomic integrity. In this review, we discuss the mechanistic interplay between all these factors, providing an integrated view of how they contribute to the observed age-related increase in radiation sensitivity. As life expectancy increases and so it does the medical intervention, it is important to highlight the benefits of radiation protection in the elderly. Thus, a deep understanding of the mechanistic processes confining the threat of aging-related radiosensitivity is currently of foremost relevance.

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Section: Impaired Dna Repair Of the Aging Cellsmentioning

confidence: 99%

Section: Impaired Dna Repair Of the Aging Cellsmentioning

confidence: 99%

Aging and radiation: bad companions

et al. 2015

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“…NHEJ becomes inefficient and more errorprone during cellular senescence, thus favoring genomic instability and higher incidence of cancer in the elderly [80,81]. Furthermore, NHEJ-mediated VDJ recombination in B lymphocytes is impaired, reducing class switch recombination efficiency and contributing to reduced humoral repertoire and impaired immunity with aging [82]. Frequency of microhomology-mediated end joining (MMEJ) increases as a compensatory mechanism; however, at the same time, it favors that more mistakes are generated [81].…”

Section: Nonhomologous End Joined (Nhej)mentioning

confidence: 99%

The Role of DNA Repair in Cellular Aging Process

Lagunas‐Rangel¹,

Bermúdez‐Cruz²

2019

DNA Repair- An Update

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Aging is defined as the time-dependent decline of functional properties. One common denominator of aging is mitochondrial dysfunction and accumulation of genetic damage throughout life. In fact, the imperfect maintenance of nuclear and mitochondrial DNA likely represents a critical contributor of aging. Each day, the integrity and stability of DNA are challenged by exogenous physical, chemical, or biological agents, as well as by endogenous processes, including DNA replication mistakes, spontaneous hydrolytic reactions, and reactive oxygen species. In this way, DNA repair systems have evolved a complex network that is collectively able of dealing with most of the damages inflicted. However, their efficiency may decrease with age and, therefore, influence the rate of aging. Thus, the purpose of this work is to summarize the recent knowledge in cellular aging process and its link with DNA repair systems, with a particular emphasis on the molecular mechanisms associated.

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Non homologous end joining-mediated DNA break repair is impaired in B lymphocytes of aging mice

Cited by 2 publications

References 59 publications

Aging and radiation: bad companions

Aging and radiation: bad companions

The Role of DNA Repair in Cellular Aging Process

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