title: Genomic instability, aging, and cellular senescence.
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.
authors.affiliation: Sam and Ann Barshop Center for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78245, USA.
authors.forename: Rita A
authors.initials: RA
authors.lastname: Busuttil
authors.forename: Martijn
authors.initials: M
authors.lastname: Dollé
authors.forename: Judith
authors.initials: J
authors.lastname: Campisi
authors.forename: Jan
authors.initials: J
authors.lastname: Vijga
mesh_terms: D000375:Aging; D000818:Animals; D017209:Apoptosis; D002478:Cells, Cultured; D016922:Cellular Senescence; D004249:DNA Damage; D005347:Fibroblasts / Q000378:metabolism; D017930:Genes, Reporter; D016678:Genome; D006801:Humans; D007763:Lac Operon; D008099:Liver / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation; D009206:Myocardium / Q000378:metabolism; D013154:Spleen / Q000378:metabolism; D013997:Time Factors