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Article

Defective mismatch binding and a mutator phenotype in cells tolerant to DNA damage.

Nature - 15 Apr 1993

Branch P, Aquilina G, Bignami M, Karran P

Abstract excerpt

Acquired resistance to alkylating agents such as N-methyl-N-nitrosourea or N-methyl-N'-nitro-N-nitrosoguanidine results from the ability to tolerate the potentially cytotoxic methylated base O6-methylguanine (m6-G) in DNA. In the absence of repair by demethylation in situ, m6-G is probably lethal through its inappropriate processing by the cell. DNA mismatch correction is an attractive candidate for the...

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Identifiers

PMID: 8464518
DOI: 10.1038/362652a0

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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Defective mismatch binding and a mutator phenotype in cells tolerant to DNA damage.PMID 8464518Read ↗

A mutator phenotype characterizes one of two complementation groups in human cells tolerant to methylation damage.Semantic proximity Read ↗

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Genetic consequences of tolerance to methylation DNA damage in mammalian cells.Semantic proximity Read ↗

Mammalian cells defective in DNA mismatch correction.Semantic proximity Read ↗

DNA mismatch repair mutants do not increase N-methyl-N'-nitro-N-nitrosoguanidine tolerance in O6-methylguanine DNA methyltransferase-deficient yeast cells.Semantic proximity Read ↗

Mechanisms of tolerance to DNA damaging therapeutic drugsSemantic proximity Read ↗

Mismatch repair as a source of mutations in non-dividing cells.Semantic proximity Read ↗

Genomic instability and tolerance to alkylating agents.Semantic proximity Read ↗

Characterisation and correction of a mammalian cell mutant defective in late step of base excision repair.Semantic proximity Read ↗

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