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The p53 tumor suppressor participates in multiple cell cycle checkpoints
Author(s) -
Giono Luciana E.,
Manfredi James J.
Publication year - 2006
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20689
Subject(s) - cell cycle , microbiology and biotechnology , mitosis , cell cycle checkpoint , biology , suppressor , cell division , dna replication , carcinogenesis , dna damage , dna , dna re replication , genetics , genome , cell , control of chromosome duplication , gene
The process of cell division is highly ordered and regulated. Checkpoints exist to delay progression into the next cell cycle phase only when the previous step is fully completed. The ultimate goal is to guarantee that the two daughter cells inherit a complete and faithful copy of the genome. Checkpoints can become activated due to DNA damage, exogenous stress signals, defects during the replication of DNA, or failure of chromosomes to attach to the mitotic spindle. Abrogation of cell cycle checkpoints can result in death for a unicellular organism or uncontrolled proliferation and tumorigenesis in metazoans (Nyberg et al., 2002). The tumor suppressor p53 plays a critical role in each of these cell cycle checkpoints and is reviewed here. J. Cell. Physiol. 209: 13–20, 2006. © 2006 Wiley‐Liss, Inc.