DNA Damage Detection by 53BP1: Relationship to Species Longevity
Autor: | Thomas D. Stamato, Silvia Marchionni, Silvana Hrelia, Antonello Lorenzini, Cristina Angeloni, Martine Bocchini, Claudio Stefanelli, Eleonora Croco, Christian Sell |
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Přispěvatelé: | Croco, Eleonora, Marchionni, Silvia, Bocchini, Martine, Angeloni, Cristina, Stamato, Thoma, Stefanelli, Claudio, Hrelia, Silvana, Sell, Christian, Lorenzini, Antonello |
Jazyk: | angličtina |
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Genome instability Aging DNA damage Longevity Cyclin A DNA Fragmentation Genomic Instability Cell Line Histones 03 medical and health sciences chemistry.chemical_compound Mice Dogs Life Expectancy Zinostatin Chiroptera Medicine Animals Humans NIMA-Related Kinases Topoisomerase II Inhibitors Micronuclei Chromosome-Defective Etoposide Neocarzinostatin Micronucleus Tests biology business.industry Cytotoxins Cell Cycle Checkpoints Fibroblasts Molecular biology 030104 developmental biology Histone 53BP1 DNA damage foci Genomic stability Longevity Micronuclei chemistry Micronucleus test biology.protein DNA fragmentation Cattle Geriatrics and Gerontology Topoisomerase-II Inhibitor business Tumor Suppressor p53-Binding Protein 1 DNA medicine.drug DNA Damage |
Popis: | 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. |
Databáze: | OpenAIRE |
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