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

We have reported previously the detection of two stable immediate-early (IE) transcripts that accumulate in cycloheximide-treated cells infected with herpesvirus saimiri (HVS). These are the 1.6-kb mRNA from the 52-kDa gene (which is homologous to the BSLF2-BMLF1 gene of Epstein-Barr virus) and the 1.3-kb mRNA from the HindIII-G fragment of virus DNA. In order to study the roles of the HVS IE gene products in the progression of a lytic infection, the promoter region of the delayed-early 110-kDa gene of HVS was sequenced, the transcription initiation site was mapped by RNase protection, and the promoter sequences were cloned upstream of the chloramphenicol acetyltransferase (CAT) gene. Sequences between -447 and +37 (relative to the 110-kDa transcription initiation site) were sufficient for response to HVS superinfection of transfected cells, but the 110-kDa promoter was activated only poorly by the 52-kDa and HindIII-G IE (IE-G) proteins in cotransfection experiments. However, a distinct region of the genome, EcoRI-D (15 kbp), was able to activate 110-kDa-CAT expression relatively efficiently in similar experiments. A 4.7-kbp PstI fragment encoding this function was isolated and sequenced, and further subcloning identified the gene encoding the EcoRI-D trans activator. This gene, which we now designate HVS.R, is homologous to the BRLF1-encoded transcriptional effector of Epstein-Barr virus.
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PMID:Regulation of the herpesvirus saimiri (HVS) delayed-early 110-kilodalton promoter by HVS immediate-early gene products and a homolog of the Epstein-Barr virus R trans activator. 185 23

Infection with human herpesvirus 6 (HHV-6) was found to up-regulate expression of human immunodeficiency virus and human T cell leukaemia virus type I (HTLV-I) long terminal repeat sequence (LTR), and herpes simplex virus type 1 (HSV-1) gD chloramphenicol acetyltransferase (CAT) constructs transfected into the T cell line, J. Jhan. Activation by HHV-6 was due to one or more viral proteins produced early in infection and, in the case of the HTLV-I LTR, was synergistic to induction mediated by the HTLV-I tax gene product. Neither the HTLV-I enhancer nor basal promoter elements of the HSV-1 gD gene were essential for activation and no increase in accumulated HTLV-I mRNA was observed due to HHV-6 infection. Induction by HHV-6 was found to be dependent on the reporter construct used, because the CAT gene and, to a lesser extent, the HSV-1 thymidine kinase gene were responsive to HHV-6 infection although no significant activation of growth hormone constructs was observed. Our results bear a strong resemblance to those obtained for the Epstein-Barr virus BMLF1 gene, indicating that the major HHV-6 trans-activator may be a homologue of this gene.
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PMID:Activation of gene expression by human herpesvirus 6 is reporter gene-dependent. 185 12

Epstein-Barr virus (EBV) latent-infection membrane protein (LMP) gene cis-acting regulatory sequences were assayed in human B lymphocytes by using chloramphenicol acetyltransferase (cat) gene expression as a reporter. The activities of progressively longer upstream elements from bases -55 to -2350 were compared. At least two positive cis-activating regulatory components (-155 to -147 and -234 to -205) upstream of the LMP promoter were defined. LMP promoter cat gene constructs were more active in a Burkitt's lymphoma cell line latently infected with the B95 EBV strain than in the same cells latently infected with the P3HR1 EBV strain. Since the P3HR1- and B95-infected cells differ in EBNA-2 and EBNA-LP expression, EBNA-2 or EBNA-LP is a likely transactivator of the LMP promoter. Probable cognate sequences for known transcription factors in the LMP promoter are discussed.
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PMID:cis-acting regulatory elements near the Epstein-Barr virus latent-infection membrane protein transcriptional start site. 215 69

Immortalization of B lymphocytes by Epstein-Barr virus (EBV) is complex and poorly understood. However, some evidence suggests that glucocorticoids influence this process. We identified a glucocorticoid-responsive element in the BamHI C fragment of EBV which we call ES-1. In glucocorticoid-treated cells, ES-1 enhanced chloramphenicol acetyltransferase gene expression from the herpes simplex virus thymidine kinase promoter, as well as the EBV Bam-C promoter, from which several latent viral gene products are transcribed. By Northern blot analysis, glucocorticoid treatment enhanced transcription from the Bam-C promoter in Jijoye cells, a Burkitt's lymphoma cell line. In addition, the DNA-binding domain of the glucocorticoid receptor bound specifically to the ES-1 region. These glucocorticoid effects on the Bam-C promoter region may provide some insight into the process of EBV immortalization.
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PMID:Identification of a glucocorticoid-responsive element in Epstein-Barr virus. 215 66

We have investigated the effect of Epstein-Barr virus nuclear antigen 1 (EBNA-1), a nuclear protein encoded by EBV, on herpes simplex virus type 1 (HSV-1) infection either in cells constitutively expressing EBNA-1 or in transient expression assays. Rat-1 cells and rat embryo fibroblasts (REF) immortalized by c-myc or E1A were transfected with a specific EBV DNA fragment coding for EBNA-1. Cloned cell lines which constitutively expressed this antigen were infected with HSV-1. Our results indicate that in EBNA-1-expressing cells, virus growth was higher than in control cells for different virus strains or rodent cell lines. This increase was maximal when cells were infected at low multiplicity, as determined by virus growth, and correlated with the stimulation of viral DNA synthesis. REF + c-myc and Vero cells were cotransfected by an EBNA-1 expression vector driven by Moloney murine leukaemia virus LTR and HSV-1 immediate-early (alpha 0) or early thymidine kinase upstream promoter regulatory regions linked to chloramphenicol acetyltransferase (CAT) coding sequences as effectors. In both cell lines, stimulation of CAT expression by EBNA-1 was observed only with the immediate-early promoter. These results suggest that EBNA-1 can transactivate immediate-early HSV-1 expression.
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PMID:Herpes simplex type 1 activation by Epstein-Barr virus nuclear antigen 1. 215 38

Several lines of evidence are compatible with the hypothesis that Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA-2) or leader protein (EBNA-LP) affects expression of the EBV latent infection membrane protein LMP1. We now demonstrate the following. (i) Acute transfection and expression of EBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased LMP1 expression in P3HR-1-infected Burkitt's lymphoma cells and the P3HR-1 or Daudi cell line. (ii) Transfection and expression of EBNA-LP alone had no effect on LMP1 expression and did not act synergistically with EBNA-2 to affect LMP1 expression. (iii) LMP1 expression in Daudi and P3HR-1-infected cells was controlled at the mRNA level, and EBNA-2 expression in Daudi cells increased LMP1 mRNA. (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB, Louckes, and BL30. (v) An EBNA-2-responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector. (vi) The EBV type 2 EBNA-2 transactivated LMP1 as well as the EBV type 1 EBNA-2. (vii) Two deletions within the EBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1, whereas a transformation-competent EBNA-2 deletion mutant did transactivate LMP1. LMP1 is a potent effector of B-lymphocyte activation and can act synergistically with EBNA-2 to induce cellular CD23 gene expression. Thus, EBNA-2 transactivation of LMP1 amplifies the biological impact of EBNA-2 and underscores its central role in EBV-induced growth transformation.
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PMID:Epstein-Barr virus nuclear antigen 2 transactivates latent membrane protein LMP1. 235 28

Transcription from the Moloney murine leukemia virus (Mo-MuLV) long terminal repeat (LTR) is inhibited in murine stem cells and induced during maturation of these cells. We have investigated whether alterations in the activity of this viral regulatory element also occur during differentiation of human myeloid leukemia cells. The Mo-MuLV LTR and the simian virus 40 (SV40) early promoter were introduced into HL-60 promyelocytes on Epstein-Barr virus-derived chloramphenicol acetyltransferase expression vectors. When these cells were induced to terminally differentiate, transcription from the Mo-MuLV LTR was induced approximately 10-fold. Expression from the SV40 promoter remained constant during differentiation of these cells. Replacing the SV40 transcriptional enhancer with the Mo-MuLV LTR transcriptional enhancer rendered the SV40 promoter inducible during differentiation. We conclude that sequences within the transcriptional enhancer of the Mo-MuLV LTR contain cis-acting elements responsible for induction of gene expression during differentiation of human myeloid cells.
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PMID:Induced expression from the Moloney murine leukemia virus long terminal repeat during differentiation of human myeloid cells is mediated through its transcriptional enhancer. 247 90

The Epstein-Barr Virus (EBV) DR promoter controlled the expression of the PstI repeat region IR4. This promoter was activated by the EBV trans-acting factor EB1, mainly at the transcriptional level, and the activation was mediated by the TATA box and two cis-acting regulatory regions, one proximal to the TATA box and one distal to the TATA box. The distal region had enhancer properties. In HeLa cells, it activated transcription from the herpes simplex virus type 1 thymidine kinase promoter linked to the chloramphenicol acetyltransferase gene when located in inverted orientation upstream of the thymidine kinase promoter or downstream of the chloramphenicol acetyltransferase gene coding sequence. This enhancer also activated transcription from the simian virus 40 early upstream regulatory elements. These results indicate that the DR These results indicate that the DR enhancer can constitutively activate heterologous promoters in HeLa cells. However, the DR enhancer was not active in EBV genome-negative B cell lines, but it became active when these cells were infected by EBV and when the expression of the EBV early genes was induced by EB1. This suggests that an EBV early gene product induces the DR enhancer activity. The DR promoter TATA box-proximal cis-acting regulatory element contained EB1-responsive sequences.
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PMID:The Epstein-Barr virus (EBV) early promoter DR contains a cis-acting element responsive to the EBV transactivator EB1 and an enhancer with constitutive and inducible activities. 253 96

The Epstein-Barr virus (EBV) BZLF1 gene product is thought to mediate the disruption of latent EBV infection. We have examined the regulatory effects of BZLF1 by studying its transactivating effects on seven different EBV promoters. We find that whereas the BZLF1 gene product increases the activity of the two early promoters, BMLF1 and BMRF1, it decreases the activity of three latent promoters (the BamHI-C and BamHI-W Epstein-Barr nuclear antigen promoters and the latent membrane protein promoter). The BZLF1-induced changes in promoter-directed chloramphenicol acetyltransferase activity occur in EBV-negative as well as EBV-positive cell lines and are accompanied by a similar change in chloramphenicol acetyltransferase mRNA. Deletion analysis of the BamHI Z fragment indicates that in a portion of the amino-terminal half of the BZLF1 gene product (amino acids 24 to 86) is not essential for positive transactivating effects but is required for down-regulating effects. Thus, different domains of the same EBV immediate-early gene product can either increase the function of EBV promoters active in productive infection or decrease the function of key promoters active in latent infection.
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PMID:The Epstein-Barr virus (EBV) BZLF1 immediate-early gene product differentially affects latent versus productive EBV promoters. 253 53

In DNA cotransfection experiments, the Epstein-Barr virus immediate-early gene product, BMLF1, stimulated the chloramphenicol acetyltransferase (CAT) activity of both latent and productive EBV promoters linked to CAT. This BMLF1-induced increase in CAT activity was out of proportion to the effect on CAT mRNA, suggesting a posttranscriptional mechanism. Furthermore, when growth hormone was used as a reporter gene instead of CAT, BMLF1 no longer functioned. Thus, the BMLF1 effect was reporter-gene dependent. The effect of the BMLF1 gene product does not then appear to be directed at promoter activation, but instead may function to increase the level of an as yet unidentified protein(s) required for Epstein-Barr virus infection.
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PMID:The Epstein-Barr virus immediate-early gene product, BMLF1, acts in trans by a posttranscriptional mechanism which is reporter gene dependent. 254 2


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