Genomic instability, aging, and cellular senescence

Rita A. Busuttil, Martijn Dollé, Judith Campisi, Jan Vijg

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Aging can be defined in practical terms as a series of time-related processes that ultimately bring life to a close. Genomic instability has been implicated as a major causal factor in aging. Here, we describe the use of a transgenic mouse model, harboring lacZ reporter genes as part of a plasmid construct integrated at one or more chromosomal locations, to study genomic instability during aging of different mouse organs and tissues as well as in mouse embryonic fibroblasts during primary culture.

Original languageEnglish (US)
Pages (from-to)245-255
Number of pages11
JournalAnnals of the New York Academy of Sciences
Volume1019
DOIs
StatePublished - 2004
Externally publishedYes

Fingerprint

Genomic Instability
Cell Aging
Aging of materials
Lac Operon
Reporter Genes
Transgenic Mice
Plasmids
Fibroblasts
Cell culture
Genes
Tissue
Mouse

Keywords

  • Aging
  • Cancer
  • DNA damage
  • Genomic integrity
  • Osidative damage

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Genomic instability, aging, and cellular senescence. / Busuttil, Rita A.; Dollé, Martijn; Campisi, Judith; Vijg, Jan.

In: Annals of the New York Academy of Sciences, Vol. 1019, 2004, p. 245-255.

Research output: Contribution to journalArticle

Busuttil, Rita A. ; Dollé, Martijn ; Campisi, Judith ; Vijg, Jan. / Genomic instability, aging, and cellular senescence. In: Annals of the New York Academy of Sciences. 2004 ; Vol. 1019. pp. 245-255.
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