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Genomic Instability, Aging, and Cellular Senescence
aSam and Ann Barshop Center for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, Texas 78245, USA bLife Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA, and Buck Institute for Age Research, Novato, California 94945, USA cGeriatric Research Education and Clinical Center, South Texas Veterans Health Care System, San Antonio, Texas 78229, USA
Address for correspondence: Jan Vijg, Sam and Ann Barshop Center for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78245. Voice: 210-562-5027; fax: 210-562-5028. vijg{at}uthscsa.edu Ann. N.Y. Acad. Sci. 1019: 245-255 (2004).
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.
Key Words: aging • cancer • oxidative damage • DNA damage • genomic integrity This article has been cited by other articles:
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