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)

Lentiviruses are known to encode factors which trans activate expression from the viral long terminal repeat (LTR); the primary trans activator is the tat gene product. One of the putative accessory genes (tat) of the bovine immunodeficiency-like virus (BIV) bears sequence similarity to other lentivirus tat genes. This finding suggests that BIV may encode a trans-activating protein capable of stimulating LTR-directed gene expression. To test this hypothesis in vitro, BIV LTR-chloramphenicol acetyltransferase (CAT) reporter gene plasmids were constructed and transfected into three cell lines established from canine, bovine, or lapine tissues that are susceptible to BIV infection. The level of BIV LTR-directed CAT gene expression was significantly elevated in BIV-infected cells compared with uninfected cells. The relatively high basal-level expression of BIV LTR-CAT in uninfected canine and bovine cell lines suggests that cellular factors play a role in regulating BIV LTR-directed gene expression. Additionally, by using a clonal canine cell line in which the BIV LTR-CAT plasmid is stably expressed, BIV LTR-directed CAT expression is elevated 15- to 80-fold by cocultivation with BIV-infected cells, supporting the notion that BIV encodes a trans activator. The relative specificity of this viral activation was assessed by coculturing the clonal BIV LTR-CAT cell line with bovine leukemia virus- or bovine syncytial virus-infected cells; these bovine retroviruses increased expression from the BIV LTR only two- to threefold. Thus, BIV LTR regulatory elements in infected cells, like those of human immunodeficiency virus type 1 and other lentiviruses, are trans activated, presumably through the action of a Tat-like protein and cellular factors.
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PMID:Bovine immunodeficiency-like virus encodes factors which trans activate the long terminal repeat. 131 91

Transactivator proteins of the bovine leukemia (BLV) and human T-lymphotropic (HTLV) viruses increase long terminal repeat (LTR)-directed viral gene expression and act as immortalizing oncogenes in tissue culture. We report here that the BLV tax gene sequence contains an enhancer-like activity. The X long open reading frame was cloned up-stream of the beta-globin promoter linked to the chloramphenicol acetyltransferase (CAT) gene. In the presence of tax sequences, up to sevenfold enhancement of CAT expression was observed. A computer-assisted homology search revealed the presence of a consensus enhancer core sequence (GTGTTGTTGGTTG) into the third exon of the 2.1-kb X mRNA. These studies demonstrate that the tax gene contains a transcriptional enhancer which could be involved in early viral gene expression in vivo.
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PMID:The bovine leukemia virus tax gene contains an enhancer sequence. 185 Aug 98

The genome of bovine leukemia virus (BLV) encodes a transcriptional trans-activator p38tax (also referred to as pXBL-I) which amplifies the virus gene expression driven by its long terminal repeat (LTR). It was proposed that activation of cellular gene expression by p38tax might be involved in the mechanism of B-cell transformation caused in vivo by BLV infection. Here, we report that the U3 region of BLV LTR contains multiple regulatory elements responsive to p38tax. A core element composing the p38tax-inducible U3 structure is suggested to be a heptanucleotide motif of 5'TGACGTCA3', the consensus sequence proposed for a cAMP-responsive element (CRE) and for the binding sites of a cellular transcription factor (ATF). Adenovirus-5 E3 and E4, c-fos and somatostatin regulatory regions containing CRE/ATF-element exhibited responsiveness to p38tax in a chloramphenicol acetyltransferase transient expression assay. These suggest that in BLV-infected cells, cellular gene expression might be induced abnormally by the virus trans-activator through ATF or ATF-like factors.
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PMID:Bovine leukemia virus trans-activator p38tax activates heterologous promoters with a common sequence known as a cAMP-responsive element or the binding site of a cellular transcription factor ATF. 254 18

The functional activity of the promoter unit contained within the long terminal repeat (LTR) of bovine leukemia virus (BLV) was examined by monitoring transient expression of a heterologous gene placed under its control. Various cell lines were transfected with recombinant plasmids carrying the bacterial chloramphenicol acetyltransferase (CAT) gene coupled to the BLV LTR (pBL-cat). Transient expression of CAT activity directed by the BLV LTR was observed only in the established BLV-producer cell lines derived from fetal lamb kidney (FLK) cells and bat lung cells. The amount of CAT activity transiently expressed in FLK-BLV cells was decreased approximately tenfold by deletion of LTR sequences located within a region 100 to 170 nucleotides upstream of the RNA start site. Surprisingly, removal of the region 50 base pairs downstream of the RNA initiation site to the 3'-end of the LTR reduced the expression of CAT activity by 87 percent. The BLV LTR thus appears to be an unusual promoter unit, functioning in a cell type-specific manner and possessing sequences on both the 5' and 3' sides of the RNA start site that influence gene expression.
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PMID:Bovine leukemia virus long terminal repeat: a cell type-specific promoter. 298 31

The ability of the sequences present in the long terminal repeats (LTRs) of human T-cell leukemia viruses type I and II (HTLV-I and HTLV-II) and of bovine leukemia virus to function as enhancer elements was investigated. Recombinant plasmids that contained the HTLV-I, HTLV-II, and bovine leukemia virus LTRs at a distance from a simian virus 40 promoter element located 5' to the bacterial gene encoding chloramphenicol acetyltransferase (EC 2.3.1.28) were constructed. We report that all three LTR sequences contain enhancer elements capable of increasing the level of gene expression directed from a distal heterologous promoter. The enhancer present in the HTLV-I LTR was active in uninfected cells of lymphoid and nonlymphoid origin. In contrast, the enhancer activity of the HTLV-II and bovine leukemia virus LTR sequences was evident only in virus-infected cells. This activity is likely due to virus-associated trans-acting transcriptional factors previously shown to be present in HTLV- and bovine leukemia virus-infected cells. The implication of these observations for virus replication and transforming activity are discussed.
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PMID:Activation of enhancer sequences in type II human T-cell leukemia virus and bovine leukemia virus long terminal repeats by virus-associated trans-acting regulatory factors. 300 24

The bovine leukemia virus, like the human T-cell leukemia viruses (HTLV-I and HTLV-II), are unusual biologically in that viral transcripts are not detected in tumors or infected tissues. The bovine leukemia virus long terminal repeat (BLV LTR) functions as a transcriptional promoter only in cell lines productively infected with BLV. Deletion mapping indicated that at least two regions of the LTR, on the 5' and 3' sides of the RNA start site, influenced gene expression. An analysis has now been made of the effects of coupling sequences from these LTR regions to a heterologous core promoter derived from the SV40 early promoter unit. Through the use of the transient expression of the bacterial chloramphenicol acetyltransferase (CAT) gene to monitor transcriptional activity in vivo, two independent, regulatory elements were identified in the BLV LTR. One was present in a fragment of 75 base pairs derived from the U3 region of the LTR and behaved much like other enhancer elements. It may be a major determinant of BLV expression in productively infected cell lines, since it enhanced transcription controlled by the heterologous core promoter only in these cells. The second element was contained in a 250-bp fragment derived from LTR sequences in the R region, located downstream from the RNA start site. Its activation of CAT expression was not dependent on BLV infection and was evident only when the fragment was located immediately downstream from the RNA start site. BLV expression thus appears to be regulated in part by a cell-specific enhancer element upstream from the core promoter and a novel sequence downstream from the RNA initiation site in the viral LTR.
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PMID:Two elements in the bovine leukemia virus long terminal repeat that regulate gene expression. 300 41

We constructed a fusion plasmid, pMX-I, by which the major open reading frame, X-I, of the bovine leukemia virus (BLV) X gene was expressed under control of the mouse metallothionein promoter. pMX-I was cotransfected into CV1 monkey kidney cells together with another construct containing the BLV long terminal repeat (LTR) linked to the chloramphenicol acetyltransferase (CAT) structural gene. The result of assay of CAT synthesis suggests that the X-I product functions as a trans-acting activation factor of the BLV LTR.
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PMID:The bovine leukemia virus X region encodes a trans-activator of its long terminal repeat. 303 Sep 87

Although the mechanism by which bovine leukemia virus (BLV) induces neoplastic transformation of the host B cells is unknown, it is likely that critical interactions between cellular DNA-binding proteins and the virus are involved. We have used DNase I protection (footprinting) assays to construct a map of protein-DNA interactions on the 5' long terminal repeat of BLV. In addition to the three cyclic AMP response elements previously reported, we have also found an NF-kappa B binding site between -118 and -70 nucleotides upstream of the RNA start site. This site binds several members of the kappa B family of proteins, including p49, p50, and p65, in both footprint and electrophoretic mobility shift assays and functions as an enhancer element when inserted upstream of the chloramphenicol acetyltransferase gene. NF-kappa B may be a critical nuclear binding protein that regulates both viral replication and key cellular genes in BLV-infected B cells.
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PMID:Identification of an NF-kappa B binding site in the bovine leukemia virus promoter. 766 5

A recombinant plasmid which contained a gene for diphtheria toxin A-chain (DT-A) under the control of the long terminal repeat (LTR) of bovine leukemia virus (BLV) (BLV-LTR) was constructed to test a novel application of liposomes as antiviral agents. The promoter activity of BLV-LTR was estimated by the chloramphenicol acetyltransferase (CAT) assay using a plasmid which contains the coding sequence of CAT under the control of BLV-LTR (pBLVCAT). When BLV-infected cells were transfected with pBLVCAT, CAT activity was detected. BLV-uninfected cell lines, however, showed no detectable CAT activity. The plasmid DNA entrapped in liposomes was added to BLV-infected cells in culture. Syncytium formation induced by BLV-infected cells was effectively suppressed by the liposomes containing the gene for DT-A under the control of BLV-LTR. Conversely, liposomes containing the gene for DT-A without a promoter showed no such effect. DT-A gene-containing liposomes with BLV-LTR did not affect formation of syncytium induced by bovine immunodeficiency virus. These observations indicate that BLV-infected cells were readily targeted on the level of gene expression. This strategy could be applied to the treatment of BLV-induced B-cell proliferation of cattle, and further to other viral/neoplastic diseases where specific gene expression is exerted.
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PMID:Suppressive effect of liposomes containing DNA coding for diphtheria toxin A-chain on cells transformed with bovine leukemia virus. 827 74

The hormone regulation of viruses has been of great interest since the discovery of glucocorticoid stimulation of mouse mammary tumor virus via a hormone response element in the viral long terminal repeat (LTR) promoter region. This report describes the investigation of the hormone responsiveness of bovine leukemia virus (BLV), an oncogenic retrovirus that infects dairy and beef cattle worldwide. It is a member of the human T cell leukemia (HTLV)/BLV group of retroviruses, which encode a protein, Tax, that is essential for regulating transcription of their own proviruses and for transforming host cells. We investigated the responsiveness of BLV to the hormones 17 beta-estradiol, progesterone, prolactin, insulin, and dexamethasone, a potent glucocorticoid. Only dexamethasone, in combination with insulin or insulin/prolactin, consistently stimulated BLV expression, as measured by reverse transcriptase activity, RNA blot hybridization (Northern blots), and CAT (chloramphenicol acetyltransferase) reporter assays of cell lines transiently or stably transfected with the BLV LTR. This effect required the presence of glucocorticoid receptors and Tax. This is the first report of hormone responsiveness in a virus of the HTLV/BLV group.
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PMID:Hormone regulation of bovine leukemia virus via the long terminal repeat. 943 16


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