Effects of p21 deletion in mouse models of premature aging

• Published in: Cell cycle (Georgetown, Tex.) Vol. 8; no. 13; pp. 2002 - 2004
• Main Authors: Benson, Erica K., Zhao, Bo, Sassoon, David A., Lee, Sam W., Aaronson, Stuart A.
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 01-07-2009
• Subjects: Aging, Premature - genetics; Animals; Antigens, Nuclear - genetics; Antigens, Nuclear - metabolism; Ataxia Telangiectasia Mutated Proteins; Binding; Biology; Bioscience; Calcium; Cancer; Cell; Cell Cycle Proteins - metabolism; Cellular Senescence; Cycle; Cyclin-Dependent Kinase Inhibitor p21 - genetics; Cyclin-Dependent Kinase Inhibitor p21 - metabolism; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Gene Knockout Techniques; Ku Autoantigen; Landes; Mice; Mice, Knockout; Organogenesis; Protein-Serine-Threonine Kinases - metabolism; Proteins; RNA - genetics; RNA - metabolism; Telomerase - genetics; Telomerase - metabolism; Tumor Suppressor Protein p53 - metabolism; Tumor Suppressor Proteins - metabolism
• ISSN: 1538-4101; 1551-4005
• DOI: 10.4161/cc.8.13.8997

An approach to investigate the role of cellular senescence in organismal aging has been to abrogate signaling pathways known to induce cellular senescence and to assess the effects in mouse models of premature aging. Recently, we reported the effect of loss of function of p21, a gene implicated in p53-induced cellular senescence, in the background of the Ku80-/- premature aging mouse (Zhao et al., EMBO reports, 2009). Here, we provide an overview of the effects of p21 deletion in different models of premature aging.