p53 and p21 regulate error-prone DNA repair to yield a lower mutation load

Regulation of mutation rates is critical for maintaining genome stability and controlling cancer risk. A special challenge to this regulation is the presence of multiple mutagenic DNA polymerases in mammals. These polymerases function in translesion DNA synthesis (TLS), an error-prone DNA repair pro...

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Bibliographic Details
Published in:	Molecular cell Vol. 22; no. 3; p. 407
Main Authors:	Avkin, Sharon, Sevilya, Ziv, Toube, Leanne, Geacintov, Nicholas, Chaney, Stephen G, Oren, Moshe, Livneh, Zvi
Format:	Journal Article
Language:	English
Published:	United States 05.05.2006
Subjects:	Animals Cyclin-Dependent Kinase Inhibitor p21 - deficiency Cyclin-Dependent Kinase Inhibitor p21 - metabolism DNA - biosynthesis DNA Repair - genetics Gene Expression Regulation, Neoplastic Humans Mice Mice, Knockout Mutagenesis - genetics Mutation - genetics Proliferating Cell Nuclear Antigen - chemistry Proliferating Cell Nuclear Antigen - metabolism Protein Binding Protein Structure, Tertiary Tumor Suppressor Protein p53 - deficiency Tumor Suppressor Protein p53 - metabolism Ubiquitin - metabolism Ultraviolet Rays
ISSN:	1097-2765
Online Access:	Get more information
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