Linked Life Data

7511991

Source:http://linkedlifedata.com/resource/pubmed/id/7511991

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-5-12
pubmed:abstractText
The role of methylation of CpG dinucleotides in the regulation of O6-methylguanine-DNA methyltransferase (MGMT) gene expression has been investigated. A previous observation, that cell lines deficient in MGMT (Mer-) are methylated in a SmaI site in the MGMT gene promoter whereas MGMT-expressing cells (Mer+) are unmethylated in the same site, has been extended to a total of 30 cell lines, tumors and normal tissues. To examine further the association between methylation in the MGMT promoter and the Mer- phenotype we have treated Mer+ and Mer- cell lines with 5-azacytidine to inhibit DNA methylation. Reduced methylation in the SmaI site coincided with induction of MGMT expression for one of three Mer- cell lines. MGMT increased several-fold further upon continued culture of the induced cells in the absence of 5-azacytidine, coincident with an abrupt increase in methylation in the body of the MGMT gene even though the SmaI site remained demethylated. These results, and those of other previous studies, suggest that methylation of sequences within the MGMT gene promoter and methylation within the body of the gene have opposite effects.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
577-82
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Effect of 5-azacytidine on expression of the human DNA repair enzyme O6-methylguanine-DNA methyltransferase.
pubmed:affiliation
Department of Molecular Pharmacology, St Jude Children's Research Hospital, Memphis, TN 38101.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't