Abstract
Sp1-DNA binding sites have been reported to be essential for basal and Tat-activated transcription of the human immunodeficiency virus type 1 long terminal repeat (LTR). The role of the Sp1 transcription factor itself in regulation of the retroviral LTR, however, has not been clearly defined. It is now known, for instance, that the Sp1-DNA binding sites function also as thyroid hormone receptor response elements (V. Desay-Yajnik and H. H. Samuels, Mol. Cell. Biol. 13:5057-5069, 1993). In this report, we present data that demonstrate a strict requirement for Sp1 for both basal transcription and Tat-mediated trans activation of the human immunodeficiency virus type 1 LTR in vitro.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenoviruses, Human / genetics
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Cell Nucleus / metabolism
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Chromatography, Ion Exchange
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Gene Expression Regulation, Viral*
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Gene Products, tat / metabolism*
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HIV-1 / genetics*
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HIV-1 / metabolism*
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HeLa Cells
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Humans
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Promoter Regions, Genetic
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RNA Polymerase II / metabolism
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Repetitive Sequences, Nucleic Acid*
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Sp1 Transcription Factor / isolation & purification
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Sp1 Transcription Factor / metabolism*
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Transcription, Genetic*
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tat Gene Products, Human Immunodeficiency Virus
Substances
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Gene Products, tat
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Sp1 Transcription Factor
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tat Gene Products, Human Immunodeficiency Virus
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RNA Polymerase II