| First Author | Vogel H | Year | 1999 |
| Journal | Proc Natl Acad Sci U S A | Volume | 96 |
| Issue | 19 | Pages | 10770-5 |
| PubMed ID | 10485901 | Mgi Jnum | J:57731 |
| Mgi Id | MGI:1345593 | Doi | 10.1073/pnas.96.19.10770 |
| Citation | Vogel H, et al. (1999) Deletion of Ku86 causes early onset of senescence in mice. Proc Natl Acad Sci U S A 96(19):10770-5 |
| abstractText | 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-PK(CS), Xrcc4, and DNA ligase IV. Here we 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. |
