Current Drug Targets

Francis J. Castellino
Kleiderer-Pezold Professor of Biochemistry
Director, W.M. Keck Center for Transgene Research
Dean Emeritus, College of Science
230 Raclin-Carmichael Hall, University of Notre Dame
Notre Dame, IN 46556
USA

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The Role of Chromatin Reorganization in the Process of Cellular Senescence

Author(s): Kaoru Tominaga and Olivia M. Pereira-Smith

Affiliation: Division of Functional Biochemistry, Department of Biochemistry, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan.

Keywords: Cell cycle, cell proliferation, chromatin, DNA damage response, histone modification, immortalization, p16 CKI, p21 CKI, Cell cycle, cell proliferation, chromatin, DNA damage response, histone modification, immortalization, p16 CKI, p21 CKI, "Cellular Senescence", aging,

Abstract:

Cellular senescence is a state of irreversible growth arrest and thought to be a tumor suppressive mechanism. In addition, it has been reported that cellular senescence may play an important role in wound healing, tissue remodeling, organismal aging and age-related diseases. This loss of ability to divide, associated with senescence, is induced by factors that are intrinsic, such as genetically defined pathways and telomere erosion, and extrinsic eg. DNA damage, oxidative stress, over-expression of oncogenes and inadequate growth conditions. The p53/p21 and RB/p16 pathways are key to the cell cycle arrest associated with cellular senescence. Extensive molecular changes occur when cells become senescent, as gene expression profiling of senescent versus young cells has demonstrated, and this is, in part, due to alterations in chromatin structure. Here, we review the molecular basis of the cell cycle arrest in cellular senescence, focusing on chromatin regulation. We also summarize our current knowledge of the role of cellular senescence in vivo.

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Article Details

VOLUME: 13
ISSUE: 13
Page: [1593 - 1602]
Pages: 10
DOI: 10.2174/138945012803529983