| Literature DB >> 32389917 |
Aoi Okawa1, Takamitsu Morioka2, Tatsuhiko Imaoka2, Shizuko Kakinuma2, Yoshihisa Matsumoto1.
Abstract
It is generally thought that younger people are more susceptible to cancer development after exposure to ionizing radiation in reference to epidemiological studies and animal experiments. However, little is known about the age-dependent alteration in DNA repair ability. In the present study, we examined the expression levels of proteins involved in the repair of DNA double-strand breaks through non-homologous end joining (NHEJ), i.e., DNA-dependent protein kinase catalytic subunit (DNA-PKcs), X-ray repair cross-complementing 4 (XRCC4) and XRCC4-like factor (XLF). We found that the expression of DNA-PKcs in brain tissues was higher in neonatal mice (1 week after birth) than in young adult mice (7 weeks after birth). In association with this, DNA double-strand breaks were repaired more rapidly in the brain tissues of neonatal mice than in those of young adult mice. The current results suggested a possible role for DNA-PKcs protecting developing brain tissues from DNA double-strand breaks.Entities:
Keywords: DNA double-strand break repair; DNA-dependent protein kinase catalytic subunit (DNA-PKcs); age dependency; carcinogenesis; non-homologous end joining (NHEJ); radiation
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Year: 2020 PMID: 32389917 PMCID: PMC7248211 DOI: 10.2183/pjab.96.014
Source DB: PubMed Journal: Proc Jpn Acad Ser B Phys Biol Sci ISSN: 0386-2208 Impact factor: 3.493