| Literature DB >> 23798034 |
Christian Garm1, Maria Moreno-Villanueva, Alexander Bürkle, Lisbeth Aagaard Larsen, Vilhelm A Bohr, Kaare Christensen, Tinna Stevnsner.
Abstract
Accumulation of DNA damage deriving from exogenous and endogenous sources has significant consequences for cellular survival, and is implicated in aging, cancer, and neurological diseases. Different DNA repair pathways have evolved in order to maintain genomic stability. Genetic and environmental factors are likely to influence DNA repair capacity. In order to gain more insight into the genetic and environmental contribution to the molecular basis of DNA repair, we have performed a human twin study, where we focused on the consequences of some of the most abundant types of DNA damage (single-strand breaks), and some of the most hazardous lesions (DNA double-strand breaks). DNA damage signaling response (Gamma-H2AX signaling), relative amount of endogenous damage, and DNA-strand break repair capacities were studied in peripheral blood mononuclear cells from 198 twins (94 monozygotic and 104 dizygotic). We did not detect genetic effects on the DNA-strand break variables in our study.Entities:
Keywords: DNA repair; double-strand break repair; gamma-H2AX; heritability; single-strand break repair; twins
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Year: 2013 PMID: 23798034 PMCID: PMC4586258 DOI: 10.1002/em.21791
Source DB: PubMed Journal: Environ Mol Mutagen ISSN: 0893-6692 Impact factor: 3.216