Abstract
The Tax transactivator of the human T cell leukemia virus type I (HTLV-I) exhibits oncogenic properties. A screen for proteins interacting with Tax yielded a complementary DNA (cDNA) encoding the human Int-6 protein. In mice, the Int-6 gene can be converted into a putative dominant negative oncogene after retroviral insertion. Here, Int-6 was localized in the cell nucleus to give a speckled staining pattern superposed to that of the promyelocytic leukemia (PML) protein. The binding of Tax to Int-6 caused its redistribution from the nuclear domains to the cytoplasm. Thus, Int-6 is a component of the PML nuclear bodies and Tax disrupts its normal cellular localization by binding to it.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Line
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Cell Nucleus / chemistry*
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Cytoplasm / chemistry
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Eukaryotic Initiation Factor-3
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Gene Products, tax / analysis
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Gene Products, tax / metabolism*
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HeLa Cells
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Humans
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Mice
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Neoplasm Proteins*
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Nuclear Proteins*
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Promyelocytic Leukemia Protein
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Proto-Oncogene Proteins / analysis
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism*
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Recombinant Fusion Proteins / metabolism
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Transcription Factors / analysis*
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Transfection
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Tumor Suppressor Proteins
Substances
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Eukaryotic Initiation Factor-3
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Gene Products, tax
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Neoplasm Proteins
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Nuclear Proteins
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Pml protein, mouse
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Promyelocytic Leukemia Protein
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Proto-Oncogene Proteins
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Recombinant Fusion Proteins
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Transcription Factors
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Tumor Suppressor Proteins
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PML protein, human