Hypersensitivity of DNA polymerase β null mouse fibroblasts reflects accumulation of cytotoxic repair intermediates from site-specific alkyl DNA lesions
- 29 October 2002
- journal article
- Published by Elsevier BV in DNA Repair
- Vol. 2 (1), 27-48
- https://doi.org/10.1016/s1568-7864(02)00184-2
Abstract
No abstract availableKeywords
This publication has 55 references indexed in Scilit:
- The lyase activity of the DNA repair protein β-polymerase protects from DNA-damage-induced cytotoxicityNature, 2000
- Protection against Methylation-induced Cytotoxicity by DNA Polymerase β-Dependent Long Patch Base Excision RepairPublished by Elsevier BV ,2000
- Role of DNA Polymerase β in the Excision Step of Long Patch Mammalian Base Excision RepairPublished by Elsevier BV ,1999
- Mammalian Abasic Site Base Excision RepairPublished by Elsevier BV ,1998
- Impairment of Proliferating Cell Nuclear Antigen-dependent Apurinic/Apyrimidinic Site Repair on Linear DNAPublished by Elsevier BV ,1998
- Requirement of mammalian DNA polymerase-β in base-excision repairNature, 1996
- Purification and Biochemical Characterization of Recombinant N-Methylpurine-DNA Glycosylase of the MouseBiochemistry, 1994
- Distribution of methyl and ethyl adducts following alkylation with monofunctional alkylating agentsMutation Research, 1990
- Reduction of the toxicity and mutagenicity of alkylating agents in mammalian cells harboring the Escherichia coli alkyltransferase gene.Proceedings of the National Academy of Sciences of the United States of America, 1986
- Molecular Biology of Mutagens and CarcinogensPublished by Springer Science and Business Media LLC ,1983