Abstract
We report that the expression of murine or human mutant p53 proteins in cells with no endogenous p53 proteins confers new or additional phenotypes upon these cells. Mutant p53 proteins expressed in cell lines lacking p53 resulted in either enhanced tumorigenic potential in nude mice ((10)3 cells) or enhanced plating efficiency in agar cell culture (human SAOS-2 cells). Also, mutant human p53 alleles, unlike the wild-type p53 protein, could also enhance the expression of a test gene regulated by the multi-drug resistance enhancer-promoter element. These data demonstrate a gain of function associated with p53 mutations in addition to the loss of function shown previously to be associated with mutations in this tumour suppressor gene.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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ATP Binding Cassette Transporter, Subfamily B, Member 1
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Animals
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Carrier Proteins / biosynthesis
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Carrier Proteins / genetics
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Cell Division / genetics
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Cell Line
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Clone Cells / transplantation
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Gene Expression Regulation / genetics
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Genes, p53*
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Humans
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Membrane Glycoproteins / biosynthesis
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Membrane Glycoproteins / genetics
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Mice
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Mice, Inbred BALB C
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Mice, Nude
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Mutation
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Neoplasms, Experimental / genetics
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Phenotype
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Species Specificity
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Tumor Cells, Cultured
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Tumor Suppressor Protein p53 / deficiency
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / physiology*
Substances
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ATP Binding Cassette Transporter, Subfamily B, Member 1
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Carrier Proteins
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Membrane Glycoproteins
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Tumor Suppressor Protein p53