Abstract
Previous reports showed transactivation of the long terminal repeat (LTR) of HIV-1 in Jurkat cells persistently infected with vaccinia virus. In this communication, electrophoretic mobility shift assays were used to characterize the elements in HIV-1 LTR which might be responsible for the mechanism of transactivation. The results indicated that two elements, those for binding NF-kB and NFAT-1, were able to interact with nuclear extracts derived from Jurkat cells persistently infected with vaccinia virus, suggesting that they may play a role in the transactivation of HIV-1 LTR.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Base Sequence
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Binding Sites
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Binding, Competitive
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Cell Line
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Cell Nucleus / metabolism*
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Cell Transformation, Viral
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DNA, Viral / metabolism
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DNA-Binding Proteins / metabolism
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Enhancer Elements, Genetic
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HIV Long Terminal Repeat*
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HIV-1 / genetics*
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Humans
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Molecular Sequence Data
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NF-kappa B / metabolism
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NFATC Transcription Factors
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Nuclear Proteins / metabolism*
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Oligodeoxyribonucleotides
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Restriction Mapping
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Substrate Specificity
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Transcription Factors / metabolism
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Transcriptional Activation*
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Vaccinia virus / genetics*
Substances
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DNA, Viral
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DNA-Binding Proteins
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NF-kappa B
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NFATC Transcription Factors
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Nuclear Proteins
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Oligodeoxyribonucleotides
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Transcription Factors