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)

Phage P2 induces the unrelated prophage P4. In this paper we show that this is due to the activation of the P4 late promoter PII by the P2 Cox protein. This is in contrast to the effects of Cox on P2, for which it is known from previous work that it acts as a repressor of the promoter Pc, which is responsible for expression of the immunity repressor C. The activator role of Cox was revealed by its effect on replication of P4 DNA and on the formation of chloramphenicol acetyltransferase when a promoterless cat gene was inserted downstream of the P4 PII promoter. DNase I protection studies revealed that the Cox protein binds to the repressor promoter Pc of phage P2 and to the promoter PII of phage P4. In the latter case the Cox protein binds upstream of the -35 region, in analogy to several other activators of promoters. A weak binding was found in the promoters Pe of phage P2 and Ple of phage P4. The Cox protein is a case of viral transactivation of the replication genes of one phage by a control protein of the other. However, the effects of the Cox protein are totally different in the two phages, repressive in one case and activating in the other.
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PMID:Activation of prophage P4 by the P2 Cox protein and the sites of action of the Cox protein on the two phage genomes. 265 31

A series of constructs that links the rat muscle creatine kinase promoter to the bacterial chloramphenicol acetyltransferase gene was generated. These constructs were introduced into differentiating mouse C2C12 myogenic cells to localize sequences that are important for up-regulation of the creatine kinase gene during myogenic differentiation. A muscle-specific enhancer element responsible for induction of chloramphenicol acetyltransferase expression during myogenesis was localized to a 159-base-pair region from 1,031 to 1,190 base pairs upstream of the transcription start site. Analysis of transient expression experiments using promoters mutated by deletion indicated the presence of multiple functional domains within this muscle-specific regulatory element. A DNA fragment spanning this region was used in DNase I protection experiments. Nuclear extracts derived from C2 myotubes protected three regions (designated E1, E2, and E3) on this fragment from digestion, which indicated there may be three or more trans-acting factors that interact with the creatine kinase muscle enhancer. Gel retardation assays revealed that factors able to bind specifically to E1, E2, and E3 are present in a wide variety of tissues and cell types. Transient expression assays demonstrated that elements in regions E1 and E3, but not necessarily E2, are required for full enhancer activity.
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PMID:The upstream muscle-specific enhancer of the rat muscle creatine kinase gene is composed of multiple elements. 276 36

The synthesis of the glutathione S-transferase Ya subunit is induced in the mammalian liver by chemicals such as phenobarbital and 3-methylcholanthrene. To study the mechanism of this induction, the 5'-flanking region of a mouse glutathione S-transferase Ya subunit gene was fused to the structural gene for chloramphenicol acetyltransferase. The fusion gene was introduced into hepatoma cells for the assay of the expressed acetyltransferase activity. At least two cis-regulatory elements were identified in the 5'-flanking region of the Ya gene: one, responsible for the basal level of expression, is present in the sequence up to -0.2 kb; another, responsible for the inducible expression by aromatic compounds such as beta-naphthoflavone and 3-methylcholanthrene, is located in the sequence from -0.2 kb to -1.6 kb. The inducible element was functional only in cells with normal aromatic compound receptors, and it retained responsiveness to beta-naphthoflavone when transfected into homologous (mouse) or heterologous (rat, human) hepatoma cells. A 150-bp region upstream from the transcription initiation site of the mouse Ya gene was investigated for cis-acting transcriptional elements that are recognized by specific DNA-binding proteins. We show by DNase I foot-printing assays using extracts from liver nuclei that the Ya gene promoter contains, in addition to the TATA and CCAAT boxes, a more distal element that binds a protein which is probably related to the family of nuclear factor 1 (NF1).
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PMID:Regulatory elements controlling the basal and drug-inducible expression of glutathione S-transferase Ya subunit gene. 277 26

Two distinct regions of the transforming growth factor-beta 1 (TGF-beta 1) promoter are responsive to autoregulation and activation by phorbol ester (12-O-tetradecanoylphorbol-13-acetate): sequences located between nucleotides -454 to -323 (first promoter) and between the two transcriptional start sites. We have now characterized in detail the induction of the second promoter (sequences between nucleotides + 1 to +271) of the TGF-beta 1 gene by both TGF-beta 1 and phorbol ester. By assaying progressively deleted mutations in the second promoter, we have found two regions responsible for the induction; each contains a phorbol ester-responsive element. In vitro transcription of the second promoter-chloramphenicol acetyltransferase chimeric genes using nuclear extracts of A-549 cells showed that deletion of the putative phorbol ester-responsive elements results in a 70-80% decrease in activity. DNase I footprinting and gel mobility shift assays showed that binding to an Sp1 site and the putative TRE elements are required for maximal expression of the second promoter region of the TGF-beta 1 gene. These results suggest that AP-1, which is capable of conferring phorbol ester or TGF-beta 1 responsiveness, is the major transcription factor involved in the second promoter-derived transcription of the TGF-beta 1 gene.
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PMID:Activation of the second promoter of the transforming growth factor-beta 1 gene by transforming growth factor-beta 1 and phorbol ester occurs through the same target sequences. 280 30

The upstream regulatory region of the human papilloma virus-16 (HPV-16) genomic DNA contains a sequence element with a large degree of homology to the partially palindromic sequence GGTACANNNTGTTCT, which is the consensus sequence of the glucocorticoid responsive elements of known genes regulated by this steroid hormone. DNase I and dimethylsulfate protection experiments reveal the binding of this sequence by rat glucocorticoid receptor protein. A 400-bp DNA segment centrally containing this sequence confers strong inducibility by dexamethasone to the promoter p97 of HPV-16 and to the Herpes simplex virus thymidine kinase promoter, as judged by chloramphenicol acetyltransferase activity and RNase protection assays. The same DNA segment, that does not contain the consensus sequences of all papilloma viruses relevant for E2 protein-mediated transcription enhancement, functions in an enhancer-like fashion in addition to its glucocorticoid responsive action. This hormone-independent transcription enhancement is absent in human MCF7 cells, but is strong in human HeLa cells where the combined activity of the constitutive and the steroid hormone-dependent enhancer elements stimulate transcription by a factor of 500. This cell type specificity of the HPV-16 enhancer may be responsible for the tissue tropism of the virus. These observations and the presence of numerous homologies to known enhancers of cellular and viral genes suggest a complex pattern of activation of the human papilloma virus-16 promoters.
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PMID:The upstream regulatory region of the human papilloma virus-16 contains an E2 protein-independent enhancer which is specific for cervical carcinoma cells and regulated by glucocorticoid hormones. 282 35

To analyze the significance of inducible DNase I-hypersensitive sites occurring in the 5'-flanking sequence of the major immediate-early gene of human cytomegalovirus (HCMV), various deleted portions of the HCMV immediate-early promoter regulatory region were attached to the chloramphenicol acetyltransferase (CAT) gene and assayed for activity in transiently transfected undifferentiated and differentiated human teratocarcinoma cells, Tera-2. Assays of progressive deletions in the promoter regulatory region indicated that removal of a 395-base-pair portion of this element (nucleotides -750 to -1145) containing two inducible DNase I sites which correlate with gene expression resulted in a 7.5-fold increase in CAT activity in undifferentiated cells. However, in permissive differentiated Tera-2, human foreskin fibroblast, and HeLa cells, removal of this regulatory region resulted in decreased activity. In addition, attachment of this HCMV upstream element to a homologous or heterologous promoter increased activity three- to fivefold in permissive cells. Therefore, a cis regulatory element exists 5' to the enhancer of the major immediate-early gene of HCMV. This element negative modulates expression in nonpermissive cells but positively influences expression in permissive cells.
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PMID:Negative and positive regulation by a short segment in the 5'-flanking region of the human cytomegalovirus major immediate-early gene. 282 27

To determine the location of sites that may be important for the function of the promoter of the epidermal growth factor (EGF) receptor gene and to characterize the factors that bind to these sites, the promoter region was analyzed by deletion analysis, exonuclease III protection and gel retardation assays with crude and fractionated nuclear extracts and DNase I footprinting using purified Sp1. Transfection of chimeric chloramphenicol acetyltransferase plasmids containing various deletions of the EGF receptor gene promoter into CV-1 cells indicated that the region between -178 and -16 (initiator ATG is +1) is sufficient for promoter activity. Exonuclease III protection assays revealed the presence of eight specific nuclear protein binding sites in the region between -481 and -16. Gel retardation assays confirmed that multiple protein binding sites exist in this region (-481 to -16) and quantitatively agree with exonuclease III protection. DNase I footprinting using purified Sp1 showed that this transcription factor can bind to four sites (-457 to -440, -365 to -286, -214 to -200, and -110 to -84) in the EGF receptor gene promoter and therefore may play a role in its regulation.
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PMID:Epidermal growth factor receptor gene promoter. Deletion analysis and identification of nuclear protein binding sites. 283 11

A cis-acting regulatory element within the gag gene of avian retroviruses has been localized by deletion analysis, and sites of protein interaction have been studied by DNase I footprinting. Unidirectional deletions were made from both the 5' and 3' ends of a 656-base-pair fragment of the gag gene of Fujinami sarcoma virus. These deletion mutants were tested for enhancer activity in a chloramphenicol acetyltransferase transient expression assay. A sharp 5' boundary for enhancer activity was observed between 776 and 786 nucleotides downstream from the transcription initiation site. In contrast, deletion from the 3' side resulted in a gradual loss of enhancer activity, reaching a near basal level of activity by nucleotide 868. Internal deletion of 76 nucleotides just downstream of the 5' boundary abolished enhancement. Mutagenesis of a consensus enhancer core sequence (GTGGTTTG) showed that this sequence was not necessary for enhancer activity in our transient assays. DNase I footprinting with both a highly purified enhancer-binding protein from rat liver (EBP20) and a partially purified chicken liver nuclear extract showed specific protection of nucleotides 813 to 872 within the localized enhancer region. Footprinting of unidirectional deletion mutants that had lost activity indicated that this binding was not sufficient to confer enhancement.
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PMID:Localization and footprinting of an enhancer within the avian sarcoma virus gag gene. 283 11

A point mutation at nucleotide 5258 in the enhancer of the polyomavirus host range mutant F441 permits productive infection of F9 embryonal carcinoma cells, which, when undifferentiated, are refractory to infection by wild-type polyomavirus. Synthetic oligonucleotides were used to construct viral genomes containing all four possible nucleotide pairs at nucleotide 5258. While all four of the viruses infected 3T6 cells efficiently, only F441, which has a guanosine in place of the wild-type adenosine in the early strand of DNA at position 5258, was able to infect F9 cells. Transfection assays with enhancer-dependent plasmid constructs expressing the chloramphenicol acetyltransferase gene under the control of the polyomavirus early promoter verified that only the F441 enhancer had any significant activity in F9 cells. DNase I footprinting showed that the F441 mutation creates a strong binding site for purified CCAAT box transcription factor, which is identical to nuclear factor 1. The three other mutations at nucleotide 5258 alter the affinity and the quality of factor binding at this site.
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PMID:Unique requirement for the PyF441 mutation for polyomavirus infection of F9 embryonal carcinoma cells. 283 8

On the basis of experiments with mutant virus and transfection with isolated genes, the herpes simplex virus immediate-early gene product ICP4 is known to positively regulate the transcription of viral early and late genes and negatively regulate expression from its own promoter. Binding of ICP4 to DNA sequences in several viral genes has been reported, yet the significance of ICP4-DNA interaction in transcriptional activation remains unclear. We have studied this problem by using the early glycoprotein D (gD) gene, which possesses a binding site at approximately -100 relative to the RNA initiation site. We linked this promoter and various mutant constructs to the chloramphenicol acetyltransferase gene in order to measure promoter activity in transient transfections both in the presence and in the absence of an ICP4-encoding plasmid. The natural promoter was activated 3.3-fold, and a deletion construct lacking the binding site was activated minimally (1.7-fold). Constructs containing multiple tandem repeats of the binding site (three or five inserts) demonstrated higher expression in the presence of ICP4 than did the natural promoter while retaining low levels of expression when unstimulated. Gel mobility shift assays and DNase I footprinting analyses indicated that ICP4 associated with multiple binding sites. In vitro transcription from a gD promoter construct containing multiple binding sites showed increased RNA synthesis in the presence of partially purified ICP4. These data provide the first direct evidence that binding of ICP4 to a specific DNA sequence in the gD gene contributes to activation of transcription.
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PMID:Role for DNA-protein interaction in activation of the herpes simplex virus glycoprotein D gene. 284 78


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