Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The hepatitis B virus X gene product trans activates transcription from a variety of viral and cellular regulatory elements. We expressed the complete, nonfused X protein in Escherichia coli and showed it to be active in trans activating a human immunodeficiency virus long terminal repeat-linked chloramphenicol acetyltransferase reporter gene.
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PMID:Hepatitis B virus X protein produced in Escherichia coli is biologically functional. 219 86

Three aspects of the involvement of tumor necrosis factor in human immunodeficiency virus (HIV) pathogenesis were examined. Tumor necrosis factor alpha (TNF-alpha) mRNA production was analyzed by polymerase chain reaction amplification in monocytic U937 cells and in a chronically HIV infected U937 cell line (U9-IIIB). TNF-alpha RNA was undetectable in U937 cells, whereas a low constitutive level was detected in U9-IIIB cells. Paramyxovirus infection induced a 5- to 10-fold increase in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with U937 cells, suggesting that HIV-infected monocytic cells produced higher levels of TNF-alpha than did normal cells after a secondary virus infection. The effects of TNF-alpha on gene expression were examined by transient expression assays using reporter chloramphenicol acetyltransferase plasmids linked to regulatory elements from the HIV long terminal repeat (LTR) and the beta interferon promoter. In U937 and Jurkat T lymphoid cells, the inducibility of the different hybrid promoters by TNF-alpha or phorbol ester varied in a cell type- and promoter context-specific manner; the levels of gene activity of NF-kappa B-containing plasmids correlated directly with induction of NF-kappa B DNA-binding activity. Although the intact beta interferon promoter was only weakly stimulated by phorbol ester or TNF-alpha, multimers of the PRDII NF-kappa B-binding domain were inducible by both agents. TNF-alpha was able to increase expression of the HIV LTR in T cells, but in monocytic cells, TNF-alpha did not induce the HIV LTR above a constitutive level of activity. This level of NF-kappa B-independent activity appears to be sufficient for virus multiplication, since TNF-alpha treatment had no effect on the kinetics of de novo HIV type 1 (HIV-1) infection and viral RNA production in U937 cells. However, in Jurkat cells, TNF-alpha dramatically enhanced the spread of HIV-1 through the cell population and increased viral RNA synthesis, indicating that in T cells HIV-1 multiplication was stimulated by TNF-alpha treatment.
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PMID:Cell-specific differences in activation of NF-kappa B regulatory elements of human immunodeficiency virus and beta interferon promoters by tumor necrosis factor. 220 23

The transient expression of hepatitis B virus (HBV) surface and "eJ" antigens caused by transfection of human hepatoblastoma HepG2 cells with HBV DNA was markedly inhibited by cotransfection with poly(I):poly(C). Cotransfection with poly(I):poly(C) also inhibited the expression of bacterial chloramphenicol acetyltransferase (CAT) gene which was under the control of either the HBV core promoter or the human immunodeficiency virus (HIV-1) long terminal repeat. This inhibition was much more pronounced on the expression of HBV-promoted CAT than HIV-promoted CAT. The uptake of reporter plasmid was not affected by cotransfected poly(I):poly(C). The inhibition was found to be at the steady-state CAT mRNA level and appeared to be specific for HBV and HIV regulatory sequences since CAT expression directed by other viral and cellular regulatory sequences was not inhibited. Cotransfection with a mixture of equal amounts of poly(I) and poly(C) had similar inhibitory effects whereas cotransfection with poly(l) or poly(C) alone, or other double-stranded ribo- or deoxyribonucleotides, did not have such strong effects. The addition of poly(l):poly(C) to the culture medium of cells transfected with these reporter plasmids caused little inhibition. Transfection with poly(l):poly(C) induced a minimal amount of intracellular interferon-alpha in HepG2 cells which may be involved in selective inhibition of HBV-and HIV-1-directed gene expression. 2-Aminopurine, an inhibitor of double-stranded RNA activated protein kinase known to block interferon gene induction by poly(l):poly(C), partially reversed the poly(l):poly(C)-induced inhibitory effect on HBV-CAT expression.
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PMID:Selective inhibition of hepatitis B virus and human immunodeficiency virus sequence-promoted gene expression by cotransfected poly(I):poly(C). 221 31

The protooncogene c-myb encodes a nuclear transcription factor that binds to DNA in a sequence-specific manner and transactivates transcription of several viral and cellular genes. The expression of c-myb is induced in mitogen-stimulated peripheral blood lymphocytes and is constitutively expressed in several CD4+ T-cell and myeloid cell lines, all of which constitute excellent targets for human immunodeficiency virus (HIV) infection and replication. We looked for the presence of Myb-binding motifs in human retroviral long terminal repeats (LTRs) and tested for Myb binding to HIV-1 LTR sequences by using a highly purified recombinant Myb protein. Our results show that HIV-1 LTR contains one high-affinity Myb-binding site along with two or more low-affinity binding sites. DNase I protection analysis as well as oligonucleotide competition experiments indicate that this binding is sequence specific. Introduction of purified Myb protein directly into HeLa cells harboring HIV-1 LTR chloramphenicol acetyltransferase vectors indicates that Myb protein transactivates HIV-1 LTR-mediated transcription. Thus, Myb protein binding to HIV LTR sequences may constitute one of the signals that regulates HIV-1 transcription.
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PMID:Myb protein binds to human immunodeficiency virus 1 long terminal repeat (LTR) sequences and transactivates LTR-mediated transcription. 223 22

Infection by human immunodeficiency virus (HIV) is followed in many cases by a clinically quiescent or latent phase that appears to continue as long as host antiviral defense is intact. This has raised the possibility that certain host susceptibility factors (i.e., environmental cofactors) might influence the progression of the disease. In this study we demonstrate that morphine can function to activate HIV/LTR-CAT fusion gene (HIV-long terminal repeat-chloramphenicol acetyltransferase) when transfected into undifferentiated human SH-SY5Y neuroblastoma cells. The stimulatory effect of morphine is amplified in SH-SY5Y cells that have been induced to differentiate first with phorbol 12-myristate 13-acetate (PMA) and is much less in cells differentiated with retinoic acid (RA). Morphine does not appreciably activate HIV/LTR-CAT expression in human MOLT-3 and other T cells. Morphine activation of HIV/LTR-CAT in the SH-SY5Y cells is not reversible by naltrexone and appears to involve a Fos/Jun signaling system. Our results suggest that narcotics such as morphine may lead to activation of latent HIV infection. This may be particularly important in tissues, such as brain, which can host latent HIV infection and which is uniquely damaged in patients with acquired immunodeficiency syndrome (AIDS) as evidenced by neuronal degeneration and dementia. We also predict that these findings may have important implications for the pathogenesis of AIDS, particularly in opiate drug abusers.
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PMID:Morphine-induced transactivation of HIV-1 LTR in human neuroblastoma cells. 225 36

A series of 5' deletions and a point mutation in the binding site for nuclear factor kappa B were introduced into the U3 region of a molecular clone of simian immunodeficiency virus from macaques (SIVmac142). The transcriptional activity of the mutated U3 regions was analyzed by transient chloramphenicol acetyltransferase assays. Two distinct regions in U3 appeared to contain important cis-acting sequences for transcriptional activity. Mutation of the single nuclear factor kappa B site in the SIVmac142 U3 region attenuated transcription in Rat-1 fibroblasts and Jurkat T cells. A second cis-acting element was localized to sequences between -162 and -114 in U3; deletion of long terminal repeat sequences up to -114 significantly attenuated transcriptional activity in Rat-1 cells. Furthermore, sequences between -162 and -114 contributed to inducibility of transcription by 1,3-phorbol myristate acetate in Jurkat T cells. Deletion of long terminal repeat sequences to -114, in addition to mutation of the nuclear factor kappa B site, was necessary to attenuate the response to 1,3-phorbol myristate acetate completely. A negative regulatory element analogous to that identified in the U3 region from the human immunodeficiency virus was not found in the U3 region from SIVmac142.
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PMID:cis-acting elements in the U3 region of a simian immunodeficiency virus. 233 31

Expression of the skeletal troponin I (sTnI) gene is regulated transcriptionally in a muscle-specific fashion. We show here that the region of the sTnI gene between -160 and +61 (relative to the transcription initiation site) is able to direct expression of the bacterial chloramphenicol acetyltransferase (CAT) gene is muscle cultures at a level approximately 100 times higher than in fibroblast cultures. RNA analysis demonstrated that transcription of the CAT gene was initiated at the same site as transcription of the endogenous sTnI gene and that CAT activity levels were approximately proportional to CAT mRNA levels. Deletion analysis demonstrated that the region between nucleotides -160 and -40 contained sequences essential for full promoter activity. Surprisingly, 3' deletion analysis indicated that the first exon (-6 to +61) of the sTnI gene was also required for full activity of the sTnI promoter in skeletal muscle cells. Chimeric promoter experiments, in which segments of the sTnI and the herpes simplex virus thymidine kinase promoter were interchanged, indicated that reconstitution of a muscle-specific promoter required inclusion of both the upstream and exon I regions of the sTnI gene. Exon I, and the region immediately upstream, showed DNase protection over sequence motifs related to those found in other genes, including the tar region of human immunodeficiency virus type 1. These results demonstrate that expression of the sTnI promoter in embryonic skeletal muscle cells requires complex interaction between two separate promoter regions, one of which resides within the first 61 transcribed nucleotides of the gene.
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PMID:Muscle-specific activity of the skeletal troponin I promoter requires interaction between upstream regulatory sequences and elements contained within the first transcribed exon. 235 14

Two human immunodeficiency virus type 1 (HIV-1) variants derived from a single parental isolate were found to differ substantially in their ability to replicate in CD4-positive cells. Using transient chloramphenicol acetyltransferase expression assays, we show that the long terminal repeat (LTR) of the better-replicating virus has significantly higher capacity than that of the companion virus to direct gene expression in T cells. Sequence data and site-specific mutagenesis experiments demonstrate that the higher LTR activity of the better-replicating HIV-1 is due to a combined effect of two mutations: (i) a point mutation in position -94 (relative to the transcriptional start site), which is located between the two subunits of the HIV-1 enhancer, and (ii) a duplication of 24 base pairs in positions -128 to -151, which was not previously known to be involved in any regulatory function. The presence of these mutations increases the basal level of the LTR-driven gene expression and does not influence the degree of induction caused by the viral tat gene product or by cell activation. Reciprocal exchange of LTRs between the respective viral DNAs results in a change of a recombinant virus replication pattern consistent with the activity of the particular LTR. These experiments suggest that the HIV-1 LTR is one of the sites which determines the functional heterogeneity of HIV-1.
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PMID:Differences in the basal activity of the long terminal repeat determine different replicative capacities of two closely related human immunodeficiency virus type 1 isolates. 237 Jun 77

We have examined the effect of the protein kinase C (PKC) inhibitor, staurosporine, on tumor necrosis factor (TNF)-induced cytotoxic action and augmentation of human immunodeficiency virus (HIV) expression on the chronically HIV-infected T-cell line, MOLT-4/HIV (HTLV-IIIB strain). Staurosporine enhanced the decrease in the number of viable cells caused by TNF treatment for 3 days (1 ng/ml of TNF, 43% decrease; 1 ng/ml of TNF + 20 nM staurosporine, 94%), whereas the cytotoxic action on that cell line induced by 10 ng/ml of 12-O-tetradecanoylphorbol-13-acetate (TPA), which was known to be an activator of PKC, was partially inhibited by staurosporine. In addition, staurosporine augmented the TNF cytotoxic activity against other cell lines including HIV-uninfected U937 cells(100 ng/ml of TNF, 53% decrease in the number of viable cells; 100 ng/ml of TNF + 5 nM staurosporine, 86%). However, staurosporine did not change the sensitivity of cells to TNF; thus, those insensitive to TNF were not changed to TNF sensitive by staurosporine. Furthermore, staurosporine did not affect the augmentative effect of TNF on HIV expression evaluated by levels of p24 antigen. Moreover, HIV long terminal repeat (LTR)-directed chloramphenicol acetyltransferase assay showed that staurosporine strongly inhibited the TPA-induced activation of HIV LTR, while that caused by TNF was little affected (10 ng/ml of TPA, 98.4% conversion; 10 ng/ml of TPA + 40 nM staurosporine, 22.2%, 1 ng/ml of TNF, 98.5%; 10 ng/ml of TNF + 40 nM staurosporine, 93.9%). These results suggest that TPA and TNF facilitate HIV replication by different pathways and that staurosporine augments TNF cytotoxicity by possible suppression of PKC activity in both HIV-infected and uninfected cells.
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PMID:Augmentation of cytotoxic effect of tumor necrosis factor on human immunodeficiency virus-infected cells by staurosporine, a potent protein kinase C inhibitor. 238 36

To investigate whether DNA viruses can augment gene expression of the human immunodeficiency virus (HIV), cotransfection experiments were carried out in which a recombinant plasmid containing the HIV long terminal repeat (LTR) linked to the chloramphenicol acetyltransferase (CAT) gene was transfected into cultured cells along with plasmids containing DNA from various distinct classes of DNA viruses. Molecular clones containing JC virus, BK virus, lymphotropic papovavirus, bovine papilloma virus, type 1 herpes simplex virus (HSV-1), and varicella-zoster virus sequences increased CAT expression directed by the HIV LTR. Trans-activation of the HIV LTR varied in different cell lines, but in each case the HIV tat gene product elicited the greatest stimulation. Primer-extension assays specific for HIV LTR mRNA revealed increased levels of steady-state RNA following transfection with HIV tat as well as with several of the DNA viruses. Virus-specific RNA expression paralleled the stimulation of CAT activity. More-than-additive effects were observed at both the RNA and protein levels when tat plus type 1 herpes simplex virus DNAs or tat plus JC virus DNAs were transfected into cells with the HIV LTR-CAT plasmid. These data suggest that coinfection of cells by HIV and some DNA viruses can stimulate the expression of HIV.
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PMID:Trans-activation of the human immunodeficiency virus long terminal repeat sequence by DNA viruses. 243 2


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