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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2005-2-3
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pubmed:abstractText |
Bcl-2 stimulates mutagenesis after the exposure of cells to DNA-damaging agents. However, the biological mechanisms of Bcl-2-mediated mutagenesis have remained largely obscure. Here we demonstrate that the Bcl-2-mediated suppression of hMSH2 expression results in a reduced cellular capacity to repair mismatches. The pathway linking Bcl-2 expression to the suppression of mismatch repair (MMR) activity involves the hypophosphorylation of pRb, and then the enhancement of the E2F-pRb complex. This is followed by a decrease in hMSH2 expression. MMR has a key role in protection against deleterious mutation accumulation and in maintaining genomic stability. Therefore, the decreased MMR activity by Bcl-2 may be an underlying mechanism for Bcl-2-promoted oncogenesis.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CDC2-CDC28 Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/CDK2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/E2F Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/MSH2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/MutS Homolog 2 Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Retinoblastoma Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1465-7392
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
7
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
137-47
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15619620-Base Pair Mismatch,
pubmed-meshheading:15619620-CDC2-CDC28 Kinases,
pubmed-meshheading:15619620-Cell Cycle Proteins,
pubmed-meshheading:15619620-Cells, Cultured,
pubmed-meshheading:15619620-Cyclin-Dependent Kinase 2,
pubmed-meshheading:15619620-DNA Repair,
pubmed-meshheading:15619620-DNA-Binding Proteins,
pubmed-meshheading:15619620-Down-Regulation,
pubmed-meshheading:15619620-E2F Transcription Factors,
pubmed-meshheading:15619620-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:15619620-Humans,
pubmed-meshheading:15619620-MutS Homolog 2 Protein,
pubmed-meshheading:15619620-Mutagenesis,
pubmed-meshheading:15619620-Mutation,
pubmed-meshheading:15619620-Neoplasms,
pubmed-meshheading:15619620-Phosphorylation,
pubmed-meshheading:15619620-Proto-Oncogene Proteins,
pubmed-meshheading:15619620-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:15619620-Retinoblastoma Protein,
pubmed-meshheading:15619620-Transcription, Genetic,
pubmed-meshheading:15619620-Transcription Factors
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pubmed:year |
2005
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pubmed:articleTitle |
Bcl-2 expression suppresses mismatch repair activity through inhibition of E2F transcriptional activity.
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pubmed:affiliation |
Department of Pharmacology, School of medicine, Chosun University, 375 Seusuk-dong, Gwangju 501-759, South Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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