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Science 5 July 1996: Vol. 273. no. 5271, pp. 63 - 67 DOI: 10.1126/science.273.5271.63
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Articles
Replicative Senescence: Implications for in Vivo Aging and Tumor
Suppression
James R. Smith
*
and
Olivia M. Pereira-Smith
Normal cells have limited proliferative potential in culture, a
fact that has been the basis of their use as a model for replicative
senescence for many years. Recent molecular analyses have identified
numerous changes in gene expression that occur as cells become
senescent, and the results indicate that multiple levels of control
contribute to the irreversible growth arrest. These include repression
of growth stimulatory genes, overexpression of growth inhibitory genes,
and interference with downstream pathways. Studies with cell types
other than fibroblasts will better define the role of cell senescence
in the aging process and in tumorigenesis.
The authors are at the Roy M. and Phyllis Gough Huffington
Center on Aging, in the Division of Molecular Virology, and in the
Departments of Cell Biology and Medicine, Baylor College of Medicine,
One Baylor Plaza, Houston, TX 77030-3498, USA.
*
To whom correspondence should be addressed.
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J. Biol. Chem.
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- Insulin-like Growth Factor-I Extends in Vitro Replicative Life Span of Skeletal Muscle Satellite Cells by Enhancing G1/S Cell Cycle Progression via the Activation of Phosphatidylinositol 3'-Kinase/Akt Signaling Pathway.
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275, 35942-35952
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- Senescent fibroblasts promote epithelial cell growth and tumorigenesis: A link between cancer and aging.
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PNAS
98, 12072-12077
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