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)

By using gel mobility shift assay, it was shown that the nuclear extract from F9 embryonal carcinoma (EC) cells contains a novel transcriptional regulatory factor, BF-H, that binds to the 5' upstream region of the early gene of polyoma virus. Two binding sites were located in the transcriptional enhancer domain "A" (nucleotide 5034-5041) and in the 5' upstream of the domain "A" (4998-5005), having a consensus motif (AAPuATGG) between them. Combination of in vitro mutagenesis with chloramphenicol acetyltransferase (CAT) assay revealed that BF-H is a positive transcriptional factor. Interestingly, the binding of BF-H disappeared after differentiation of F9 cells by treatment with retinoic acid, whereas BF-H was present in the F9 cells differentiated with both retinoic acid and dibutyryl cyclic AMP (dbcAMP). These observations suggest that BF-H regulates the expression of genes in a developmental stage-specific manner in early embryos of the mouse.
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PMID:A novel transcriptional regulatory factor that binds to the polyoma virus enhancer in a developmental stage-specific manner. 216 3

Stromelysin is a member of the metalloproteinase family which plays an important role in extracellular matrix remodelling during many normal and disease processes. We show here that in polyomavirus-transformed rat embryo fibroblast cells (PyT21), the transcription from the stromelysin gene is repressed by the vitamin A derivative retinoic acid (RA). Furthermore, expression vectors encoding the human RA receptors hRAR-alpha, hRAR-beta and hRAR-gamma repress chloramphenicol acetyltransferase (CAT) expression from stromelysin promoter-CAT gene expression vectors in RA-treated PyT21 and human HeLa cells, as determined by transient transfection assays. Through mutation and deletion analysis, we show that the RA dependent repression is mediated by a 25 bp region from nucleotide positions -72 to -48 of the rat stromelysin 5'-flanking DNA sequence. Further mutation analysis of this region indicates that the DNA sequence required for RA dependent repression colocalizes with an AP1 binding site which is essential for promoter activity. We show also that RA represses the transcriptional activity of a reporter gene containing a TPA responding AP1 binding site driving the HSV tk promoter. Thus the RAR-RA complex appears to repress transcription of the stromelysin gene by blocking activation by positive regulatory factors. However, we found no evidence supporting the possibility that the RA dependent repression could be due to RAR binding to the AP1 binding site or to the AP1 components c-fos and c-jun.
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PMID:Negative regulation of the rat stromelysin gene promoter by retinoic acid is mediated by an AP1 binding site. 217 52

Collagenase production by synovial fibroblast-like cells (synoviocytes) plays a major role in cartilage and bone destruction in rheumatoid arthritis. Interleukin-1 (IL-1) increases collagenase secretion by elevating the steady state levels of collagenase mRNA in cultured rheumatoid synoviocytes, while all-trans-retinoic acid (RA) has the opposite effect. We have studied the regulation of collagenase gene transcription by IL-1 and RA in synoviocytes by transient transfection of plasmid constructs containing deletion mutants of the 5'-flanking region of the collagenase gene or the isolated phorbol ester-responsive element ligated to a chloramphenicol acetyltransferase reporter gene. We show that the phorbol ester-responsive element of the collagenase gene mediates both positive and negative regulatory effects, respectively, of IL-1 and RA on transcription. In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. These results suggest that RA inhibits collagenase transcription at least in part through inhibition of c-fos.
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PMID:Interleukin-1 stimulates and all-trans-retinoic acid inhibits collagenase gene expression through its 5' activator protein-1-binding site. 217 24

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

The retinoic acid (RA)-associated differentiation of murine F9 teratocarcinoma stem cells results in dramatic changes in gene expression. The cellular gene encoding the B1 subunit of the extracellular matrix protein laminin is transcriptionally activated by RA, and its transcription is further enhanced by N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate (Bt2cAMP) during the differentiation of F9 stem cells into extraembryonic parietal endoderm cells. We now report that expression vectors encoding the human RA receptors RAR-alpha, RAR-beta, and RAR-gamma can activate chloramphenicol acetyltransferase (CAT) expression from laminin B1 promoter/CAT expression vectors (e.g., p1.6LAMCAT) in RA-treated F9 cells, as measured in a transient transfection assay. Bt2cAMP does not further enhance the RA-associated increase in CAT activity. Through the use of deletion and mutation analyses, the RA-responsive element (RARE) of the murine laminin B1 gene has been defined as a 46-base-pair element between -477 and -432 of the laminin B1 5' flanking region. Insertion of a region of DNA containing this RARE in either orientation into a thymidine kinase promoter/CAT expression vector causes CAT expression to be activated 5- to 9-fold by the cotransfected human RAR-alpha or RAR-beta constructs in RA-treated F9 cells, and this RARE also functions in human HeLa cells. In contrast, this RARE in the p1.6LAMCAT vector does not activate CAT expression when cotransfected into F9 stem cells with the c-erbA gene in the presence of thyroid hormone. This suggests that the laminin B1 gene is activated by RA but not by thyroid hormone in vivo.
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PMID:A retinoic acid-responsive element is present in the 5' flanking region of the laminin B1 gene. 255 99

UMR 201 is a nontransformed rat clonal cell line derived from neonatal calvaria with phenotypic characteristics of preosteoblasts. Retinoic acid strongly induces expression of alkaline phosphatase and its mRNA in these cells. Dexamethasone substantially reduced the retinoic acid-induced expression of alkaline phosphatase. This apparent interaction between dexamethasone and retinoic acid effects raised the possibility that interactions may extend to other osteoblast-related phenotypic characteristics in UMR 201 cells. Treatment with dexamethasone resulted in a decrease in the expression of mRNA for pro-alpha 1(I) collagen, but upon coincubation with 1 microM retinoic acid for 24 h, the decrease in mRNA for pro-alpha 1(I) collagen was abrogated. Dexamethasone (Dex) treatment caused a dose-dependent increase in osteonectin mRNA, half maximally effective between 1 nM and 10 nM Dex. One micromolar of retinoic acid alone led to a small increase in expression of osteonectin mRNA but prevented any further increase when Dex was added to retinoic acid-treated cells. To study transcriptional control, osteonectin genomic fragments were linked to the bacterial reporter gene, chloramphenicol acetyltransferase, and introduced by transfection into UMR 201 cells. Dexamethasone increased the transcriptional activity of an osteonectin-chloramphenicol acetyltransferase construct; 100 nM Dex resulted in a 3-fold increase over control cells which was attenuated when 1 microM retinoic acid was added to the incubation, while retinoic acid alone resulted in a 2-fold increase in transcriptional activity. Finally, it was noted that coincubation with retinoic acid and Dex stimulated the proliferation of UMR 201 cells when compared with either treatment alone. This study shows the potential importance of hormonal interactions in the expression of osteoblast function.
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PMID:Opposing influences of glucocorticoid and retinoic acid on transcriptional control in preosteoblasts. 262 42

We have investigated the role of 5'-flanking DNA sequences in regulating the expression of the murine Sparc (osteonectin) gene in parietal endoderm cells and in F9 embryonal carcinoma cells induced to differentiate into parietal endoderm with retinoic acid and cyclic AMP. Varying lengths of flanking sequences extending up to 3.0 kilobase pairs 5' of the transcription initiation site were linked to the bacterial chloramphenicol transacetylase gene in the Bluescript M13- vector. The constructs were tested in transient assays, using a beta-galactosidase plasmid as a transfection control. Sequences between 78 and 169 base pairs upstream of the cap site are the minimum required for cell-type specific promoter activity; this region is dominated by two oligopurine/oligopyrimidine stretches or "GAGA" boxes and is highly conserved between the mouse and bovine genes. Addition of the sequence between -169 and -449, which includes part or all of a third GAGA box, results in increased parietal endoderm specific transcription, up to a maximum of 6.3-fold higher than in undifferentiated F9 cells. Further addition of sequences between -449 and -638 markedly reduces promoter activity in both cell types but parietal endoderm-specific activity is restored in constructs containing 2.2 and 3.0 kilobase pairs of flanking DNA. In addition, we have identified sequences related to the consensus sequence for steroid response elements, one of which is able to confer progesterone-enhanced transcription when tested with a heterologous promoter in steroid responsive cells. These results suggest that negative and positive elements normally interact to regulate the temporal and tissue-specific patterns of Sparc gene transcription seen in vivo.
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PMID:Evidence for positive and negative regulatory elements in the 5'-flanking sequence of the mouse sparc (osteonectin) gene. 274 36

From a mouse genomic DNA library we have isolated sequences containing the entire coding region for histone H1(0) mRNA, flanked by several kb at both the 3' and 5' ends. Deletions of the 5' upstream region ligated to the chloramphenicol acetyltransferase (CAT)-encoding gene as a reporter, have shown that a region from bp -400 to -600 is necessary and sufficient for efficient transcription. We have also shown that treatment of F9 teratocarcinoma cells with retinoic acid and cyclic AMP (which differentiates F9 cells to parietal endoderm) clearly increases CAT activity several times over the level found in untreated F9 cells. This increase was observed in transient, as well as in stably transfected cells. Analysis of the deletions in differentiating cells indicates that the element responsible for the observed increase in CAT activity, is contained within the first 700 bp upstream from the H1(0) mRNA cap site.
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PMID:Cloning and characterization of the mouse histone H1(0) promoter region. 280 18

Murine embryonal carcinoma F9 cells, which do not express appreciable levels of major histocompatibility complex (MHC) class I mRNA, start to express the mRNA and proteins upon differentiation induced by retinoic acid (RA). To investigate the molecular mechanism of this regulation, we examined in F9 cells transient expression of the chloramphenicol acetyltransferase (CAT) gene directed by the 5' flanking region of a MHC class I gene, H-2Ld. The native 1.4-kilobase H-2Ld 5' upstream region gave very low CAT activity in undifferentiated F9 cells. Deletion between positions -210 and -135 relative to the cap site resulted in a 4- to 5-fold increase in CAT activity as compared with constructs containing the region. However, all of these constructs, regardless of the deletion, expressed comparable CAT activity in differentiated F9 cells. These data suggest the presence of a negative cis-acting element that is under developmental control. Further analysis revealed that the sequence conferring the negative regulation resides between positions -195 and -161. This region, highly conserved among the MHC class I genes, is found to be capable of increasing CAT activity in NIH 3T3 cells that express the class I genes constitutively. Further, this regulatory sequence, when connected to the simian virus 40 promoter, produced repressive and enhancing effects in F9 and NIH 3T3 cells, respectively. Based on these results, we suggest that the expression of MHC class I genes during development involves switching from negative to positive regulation dictated by the class I regulatory element located between positions -195 and -161.
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PMID:Negative regulation of the major histocompatibility class I gene in undifferentiated embryonal carcinoma cells. 346 24

The regulation of the collagen II gene was investigated by transfecting plasmids containing potential regulatory sequences of this gene coupled to the gene for chloramphenicol acetyltransferase (CAT) into various cells. The 5' flanking region of this gene functioned as a weak promoter when transfected into chicken chondrocytes or fibroblasts. Inclusion of an 800-base fragment from the first intron, however, increased transcription of CAT approximately 18-fold in chicken chondrocytes and in differentiating limb bud cells but not in fibroblasts, myoblasts, muscle-derived fibroblasts, or teratocarcinoma cells. Furthermore, this fragment was active when placed either upstream or downstream of the CAT gene and when present in either orientation. The activity of this enhancer was examined in relation to differentiation by using "micromass" culture of limb bud mesenchyme cells undergoing chondrogenesis. In this system, no response to the enhancer was observed in undifferentiated limb bud mesenchyme cells. Following differentiation into chondrocytes, a 13-fold enhancer effect was observed in these cells. Finally, all-trans-retinoic acid, a known teratogen, dramatically suppressed enhancer activity in chondrocytes and differentiating limb bud mesenchyme cells. These results suggest that the collagen II gene contains an enhancer element in the first intron that is involved in cell-specific expression.
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PMID:Identification of a phenotype-specific enhancer in the first intron of the rat collagen II gene. 348 May 15


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