Linked Life Data

8464518

Source:http://linkedlifedata.com/resource/pubmed/id/8464518

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6421
pubmed:dateCreated
1993-5-6
pubmed:abstractText
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 processing function because although it is replicated, m6-G has no perfect complementary base. Thus, m6-G in DNA might provoke abortive mismatch repair and tolerance could subsequently arise through loss of a mismatch repair pathway. Mismatch correction helps maintain genomic fidelity by removing misincorporated bases and deaminated 5-methylcytosine from DNA, and its loss by mutation confers a mutator phenotype on Escherichia coli. Here we describe human and hamster cell lines that are tolerant to N-methyl-N-nitrosourea and are defective in a DNA mismatch binding activity. The loss of this activity, which acts on G.T mispairs, confers a mutator phenotype.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
362
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
652-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Defective mismatch binding and a mutator phenotype in cells tolerant to DNA damage.
pubmed:affiliation
Imperial Cancer Research Fund, Clare Hall Laboratories, South Mimms, Herts, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't