Biochem Biophys Res Commun. 1996 Mar 18;220(2):411-7. Unique Identifier
We investigated the effect of tannic acid, a potent inhibitor of
poly(ADP-ribose) glycohydrolase, on human viral gene transcription, by
using chloramphenicol acetyl transferase (CAT) assay experiments
transfecting Jurkat cells with CAT reporter constructs that contain the
promoter region of human immunodeficiency virus (HIV) or of human T-cell
leukemia virus type I (HTLV-1). The activity of HIV promoter induced by
treatment with 12-O-tetradecanoylphorbol-13-acetate was suppressed by
the addition of tannic acid. On the other hand, HTLV-1 promoter activity
induced by the p40(tax) expression plasmid was not affected by tannic
acid treatment. Deletion analysis of the HIV promoter revealed that a
30-bp element located immediately upstream of NF-kappa B motifs was
responsible for the suppressive effect of tannic acid. This was
supported by the observations that the negative effect of tannic acid
was introduced to tannic acid-non-responsive thymidine kinase promoter
by the insertion of this element 5'-upstream of the promoter.
Base Sequence Chloramphenicol Acetyltransferase/GENETICS Gene Deletion
Human HIV/*GENETICS HTLV-I/GENETICS Molecular Sequence Data
*Promoter Regions (Genetics) Repetitive Sequences, Nucleic Acid
Support, Non-U.S. Gov't T-Lymphocytes/*VIROLOGY Tannic
Acid/*PHARMACOLOGY Tetradecanoylphorbol Acetate/*PHARMACOLOGY
Transcription, Genetic/*DRUG EFFECTS Transfection Tumor Cells,
Cultured JOURNAL ARTICLE