title: Transcriptional activation from the long-terminal repeat of human immunodeficiency virus in vitro.
abstract: The mechanism of trans-acting regulation of transcription from the long terminal repeat (LTR) of human immunodeficiency virus (HIV) has been investigated. The roles of the cis-acting elements within HIV LTR, as well as the trans-acting factors present in HIV-infected cells, have been evaluated by an in vitro transcription system. Our observations indicate that both the sequence downstream from the CAP site of HIV LTR (located at nucleotide positions +1 to +56; called the TAR element) and the GC boxes (-77 to -45) are required for full transcriptional stimulation and that both the virus-encoded tat protein and one or more cellular factors might be involved. These results demonstrate the presence of a combinatorial regulation of HIV transcription by multiple factors, which may confer the provirus with greater flexibility in regulated viral gene expression.
authors.affiliation: Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
authors.forename: T
authors.initials: T
authors.lastname: Okamoto
authors.forename: T
authors.initials: T
authors.lastname: Benter
authors.forename: S F
authors.initials: SF
authors.lastname: Josephs
authors.forename: M R
authors.initials: MR
authors.lastname: Sadaie
authors.forename: F
authors.initials: F
authors.lastname: Wong-Staal
mesh_terms: D001667:Binding, Competitive; D002467:Cell Nucleus / Q000378:metabolism; D002872:Chromosome Deletion; D002874:Chromosome Mapping; D004279:DNA, Viral / Q000378:metabolism; D015967:Gene Expression Regulation, Viral; D005814:Genes, Viral; D015497:HIV-1 / Q000235:genetics*; D006367:HeLa Cells / Q000378:metabolism; D006801:Humans; D011401:Promoter Regions, Genetic; D012091:Repetitive Sequences, Nucleic Acid; D014158:Transcription, Genetic
chemical_list: D004279:DNA, Viral