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DNA Damage Detection by 53BP1: Relationship to Species Longevity
Journal article   Open access   Peer reviewed

DNA Damage Detection by 53BP1: Relationship to Species Longevity

Eleonora Croco, Silvia Marchionni, Martine Bocchini, Cristina Angeloni, Thomas Stamato, Claudio Stefanelli, Silvana Hrelia, Christian Sell and Antonello Lorenzini
The journals of gerontology. Series A, Biological sciences and medical sciences, v 72(6), pp 763-770
01 Jun 2017
PMID: 27573809
url
https://doi.org/10.1093/gerona/glw170View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

Animals Cattle Cell Cycle Checkpoints Cell Line Chiroptera Cyclin A - metabolism Cytotoxins - toxicity DNA Damage DNA Fragmentation Dogs Etoposide - toxicity Fibroblasts - drug effects Fibroblasts - metabolism Genomic Instability Histones - metabolism Humans Life Expectancy Longevity Mice Micronuclei, Chromosome-Defective Micronucleus Tests NIMA-Related Kinases - metabolism Topoisomerase II Inhibitors - toxicity Tumor Suppressor p53-Binding Protein 1 - metabolism Zinostatin - toxicity
In order to examine potential differences in genomic stability, we have challenged fibroblasts derived from five different mammalian species of variable longevity with the genotoxic agents, etoposide and neocarzinostatin. We report that cells from longer-lived species exhibit more tumor protein p53 binding protein 1 (53BP1) foci for a given degree of DNA damage relative to shorter-lived species. The presence of a greater number of 53BP1 foci was associated with decreased DNA fragmentation and a lower percentage of cells exhibiting micronuclei. These data suggest that cells from longer-lived species have an enhanced DNA damage response. We propose that the number of 53BP1 foci that form in response to damage reflects the intrinsic capacity of cells to detect and respond to DNA harms.

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