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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
25
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pubmed:dateCreated |
2004-6-4
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pubmed:abstractText |
We have studied the mechanism of mutant p53-mediated oncogenesis using several tumor-derived mutants. Using a colony formation assay, we found that the majority of the mutants increased the number of colonies formed compared to the vector. Expression of tumor-derived p53 mutants increases the rate of cell growth, suggesting that the p53 mutants have 'gain of function' properties. We have studied the gene expression profile of cells expressing tumor-derived p53-D281G to identify genes transactivated by mutant p53. We report the transactivation of two genes, asparagine synthetase and human telomerase reverse transcriptase. Quantitative real-time PCR confirms this upregulation. Transient transfection promoter assays verify that tumor-derived p53 mutants transactivate these promoters significantly. An electrophoretic mobility shift assay shows that tumor-derived p53-mutants cannot bind to the wild-type p53 consensus sequence. The results presented here provide some evidence of a possible mechanism for mutant p53-mediated transactivation.
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pubmed:grant |
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0950-9232
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
27
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4430-43
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15077194-Amino Acid Substitution,
pubmed-meshheading:15077194-Aspartate-Ammonia Ligase,
pubmed-meshheading:15077194-Cell Division,
pubmed-meshheading:15077194-Cell Line, Tumor,
pubmed-meshheading:15077194-Cell Transformation, Neoplastic,
pubmed-meshheading:15077194-Consensus Sequence,
pubmed-meshheading:15077194-DNA-Binding Proteins,
pubmed-meshheading:15077194-Gene Expression Profiling,
pubmed-meshheading:15077194-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:15077194-Genes, Tumor Suppressor,
pubmed-meshheading:15077194-Genes, p53,
pubmed-meshheading:15077194-Humans,
pubmed-meshheading:15077194-Mutation, Missense,
pubmed-meshheading:15077194-Neoplasms,
pubmed-meshheading:15077194-Nuclear Proteins,
pubmed-meshheading:15077194-Point Mutation,
pubmed-meshheading:15077194-Promoter Regions, Genetic,
pubmed-meshheading:15077194-Protein Binding,
pubmed-meshheading:15077194-Protein Structure, Tertiary,
pubmed-meshheading:15077194-Recombinant Fusion Proteins,
pubmed-meshheading:15077194-Structure-Activity Relationship,
pubmed-meshheading:15077194-Telomerase,
pubmed-meshheading:15077194-Transcriptional Activation,
pubmed-meshheading:15077194-Tumor Stem Cell Assay,
pubmed-meshheading:15077194-Tumor Suppressor Protein p53,
pubmed-meshheading:15077194-Tumor Suppressor Proteins
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pubmed:year |
2004
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pubmed:articleTitle |
Tumor-derived p53 mutants induce oncogenesis by transactivating growth-promoting genes.
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pubmed:affiliation |
Department of Biochemistry and the Massey Cancer Center, Virginia Commonwealth University, PO Box 980614, Richmond, VA 23298, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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