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53BP1 contributes to a robust genomic stability in human fibroblasts
Journal article   Open access

53BP1 contributes to a robust genomic stability in human fibroblasts

Lauren S. Fink, Michaela Roell, Emanuela Caiazza, Chad Lerner, Thomas Stamato, Silvana Hrelia, Antonello Lorenzini and Christian Sell
Aging (Albany, NY.), v 3(9), pp 836-845
01 Sep 2011
PMID: 21931182
url
https://doi.org/10.18632/aging.100381View
Published, Version of Record (VoR)CC BY V4.0 Open

Abstract

Cell Biology Geriatrics & Gerontology Life Sciences & Biomedicine Science & Technology
Faithful repair of damaged DNA is a crucial process in maintaining cell viability and function. A multitude of factors and pathways guides this process and includes repair proteins and cell cycle checkpoint factors. Differences in the maintenance of genomic processes are one feature that may contribute to species-specific differences in lifespan. We predicted that 53BP1, a key transducer of the DNA damage response and cell cycle checkpoint control, is highly involved in maintaining genomic stability and may function differently in cells from different species. We demonstrate a difference in the levels and recruitment of 53BP1 in mouse and human cells following DNA damage. In addition, we show that unresolved DNA damage persists more in mouse cells than in human cells, as evidenced by increased numbers of micronuclei. The difference in micronuclei seems to be related to the levels of 53BP1 present in cells. Finally, we present evidence that unresolved DNA damage correlates with species lifespan. Taken together, these studies suggest a link between recruitment of 53BP1, resolution of DNA damage, and increased species lifespan.

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Cell Biology
Geriatrics & Gerontology
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