Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Epstein-Barr virus BZLF1 gene product (ZEBRA) is a transcriptional activator whose expression in latently infected B cells is sufficient to induce the viral lytic cycle. Since there is no transcription of BZLF1 during latency, we carried out experiments to determine whether cis-acting negative elements in the BZLF1 promoter contribute to the lack of expression during this phase of the virus cycle. A series of deletion plasmids encompassing positions -551 to +14 of the BZLF1 promoter region were constructed and tested for the ability to drive chloramphenicol acetyltransferase (CAT) gene expression in the absence of inducing agents such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and anti-immunoglobulin. Expression from the intact 551-bp region was very weak in most of the cell lines tested, but deletion of 165 bp from the 5' end caused a sevenfold increase in expression of CAT. Within these 165 bp, a minimal 48-bp region was sufficient to down regulate the expression of a simian virus 40/CAT fusion plasmid. The 48-bp negative element consists of 7-bp dyad symmetry elements separated by 27 bp. The rightmost half of the dyad symmetry element partially overlaps a region which has a 14-of-15-bp homology to the human cytoskeletal gamma-actin promoter.
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PMID:Negative regulation of the BZLF1 promoter of Epstein-Barr virus. 164 87

Tannic acid, which comprises polyphenolic compounds from tea leaves, suppresses the glucocorticoid-induced gene expression of mouse mammary tumor virus (MMTV) integrated into 34I cells. To investigate whether this suppression is due to promoter responsiveness to tannic acid, we performed chloramphenicol acetyltransferase analysis transfecting a MMTV promoter containing a chloramphenicol acetyltransferase expression vector into mouse fibroblast L929 cells. Deletion analysis of the promoter region revealed that a 50-base pair (bp) region located downstream of the TATA element is responsible for the suppressive effect of tannic acid. The tannic acid-sensitive suppressibility was introduced into a thymidine kinase promoter by inserting the 50-bp region into the region on the 5'-upstream side of the promoter. Detailed point mutation analyses revealed that two elements, a 13-bp element and an ACTG motif in the 50-bp region, contribute to tannic acid sensitivity and promoter repressibility, respectively. Interestingly, this repressive ACTG motif is found in the human immunodeficiency virus promoter, the activity of which is also suppressed by tannic acid (Uchiumi, F., Maruta, H., Inoue, J., Yamamoto, T., and Tanuma, S. (1996) Biochem. Biophys. Res. Commun. 220, 411-417). Furthermore, electrophoretic mobility shift analysis revealed that a protein factor(s) in nuclear extracts from L929 cells binds to the 50-bp region in a sequence-specific manner and that the amount of DNA-protein complex is increased by tannic acid treatment. Moreover, the negative regulatory sequence ACTG and the tannic acid-sensitive 13-bp element in this region were shown to be responsible for the formation of the DNA-protein complex by electrophoretic mobility shift analysis and footprint analyses. These findings suggest that the suppressive effect of tannic acid on MMTV gene expression is mediated by a protein factor(s) that binds to the negative regulatory element containing the common ACTG motif in a cooperative manner with the tannic acid-sensitive 13-bp element.
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PMID:Identification and characterization of a tannic acid-responsive negative regulatory element in the mouse mammary tumor virus promoter. 957 8