Deletion of Ku86 causes early onset of senescence in mice

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DNA double-strand breaks formed during the assembly of antigen receptors or after exposure to ionizing radiation are repaired by proteins important for nonhomologous end joining that include Ku86, Ku70, DNA-PKCS, Xrcc4, and DNA ligase IV. Here me show that ku86-mutant mice, compared with control littermates, prematurely exhibited age-specific changes characteristic of senescence that. include osteopenia, atrophic skin, hepatocellular degeneration, hepatocellular inclusions, hepatic hyperplastic foci, and age-specific mortality. Cancer and likely sepsis (indicated by reactive immune responses) partly contributed to age-specific mortality for both cohorts, and both conditions occurred earlier in ku86(-/-) mice. These data indicate that Ku86-dependent chromosomal metabolism is important for determining the onset of age-specific changes characteristic of senescence in mice.
Publisher
NATL ACAD SCIENCES
Issue Date
1999-09
Language
ENG
Article Type
Article
Keywords

DNA-REPAIR; V(D)J RECOMBINATION; SACCHAROMYCES-CEREVISIAE; SYNDROME PROTEIN; LIFE-SPAN; BRCA2; DEFICIENT; MUTATION; CANCER; CELLS

Citation

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.96, no.19, pp.10770 - 10775

ISSN
0027-8424
DOI
10.1073/pnas.96.19.10770
URI
http://hdl.handle.net/10203/74827
Appears in Collection
BS-Journal Papers(저널논문)
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