Waga, S., Li, R., Stillman, B. (April 1997) p53-induced p21 controls DNA replication. Leukemia, 11 Sup. pp. 321-3. ISSN 0887-6924 (Print)
Abstract
The p21 protein, a regulator of cyclin-dependent kinases (CDKs), has been thought to be one of the key proteins to function in cell proliferation suppression upon DNA damage. In normal cells but not in many tumor cells, p21 forms a quaternary complex with a cyclin, a CDK and the proliferating cell nuclear antigen (PCNA), one of the DNA replication and repair factors, suggesting that this complex might play an important role in maintaining the integrity of the genome. Here, we have focused on the p21-PCNA interaction in the context of DNA replication or DNA repair, presenting the data from both in vitro and in vivo studies of the p21 function.
Item Type: | Paper |
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Uncontrolled Keywords: | Antigens Viral Tumor biosynthesis genetics Cell Division Cell Line Cyclin-Dependent Kinase Inhibitor p21 Cyclin-Dependent Kinases metabolism Cyclins metabolism DNA Repair DNA Replication Enzyme Inhibitors metabolism Homeostasis Humans Plasmids Proliferating Cell Nuclear Antigen metabolism Simian virus 40 genetics/physiology Tumor Suppressor Protein p53 metabolism |
Subjects: | bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > DNA replication bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > enzymes > kinase |
CSHL Authors: | |
Communities: | CSHL labs > Stillman lab |
Highlight: | Stillman, Bruce W. |
Depositing User: | CSHL Librarian |
Date: | April 1997 |
Date Deposited: | 17 Feb 2012 20:41 |
Last Modified: | 20 Jun 2017 19:33 |
URI: | https://repository.cshl.edu/id/eprint/25129 |
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