Transcriptional activation from the long-terminal repeat of human immunodeficiency virus in vitro.
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.
Okamoto
T
T
Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
Benter
T
T
Josephs
S F
SF
Sadaie
M R
MR
Wong-Staal
F
F
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
D004279:DNA, Viral