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)

Angiotensinogen is a precursor of the multifunctional octapeptide hormone, angiotensin II. We have isolated the overlapping clones containing angiotensinogen gene locus from C57BL/6 mouse genomic DNA library and analyzed them by restriction enzyme mapping. The gene exhibited a structural organization similar to those of the human, rat and balb/c mouse angiotensinogen genes. Using a genomic DNA fragment of the mouse angiotensinogen gene as a probe, we have investigated the tissue distribution of angiotensinogen messenger RNA (mRNA) in C57BL/6 mouse. The angiotensinogen mRNA was highest in the liver and detectable in such tissues as brain, kidney, submandibular gland, ovary and heart. However, it was undetectable in lung and spleen under the condition used. Optimal alignments of the 5'-flanking regions among the human, rat and mouse angiotensinogen genes disclosed several deletions in the mouse sequence. To assay the promoter activity, the 5'-flanking region of the mouse angiotensinogen gene was ligated to the bacterial chloramphenicol acetyltransferase (CAT) gene, then transfected into different cultured cells. The angiotensinogen gene sequences elicited preferential expression of CAT activity when introduced into HepG2 cells derived from liver and 293 cells from kidney but not in HeLa cells from uterus, suggesting the presence of a cell type-specific promoter within the sequences. These findings on the structure and expression of the mouse angiotensinogen gene should prove useful in studying the function and control of the angiotensin.
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PMID:Structure and expression of the mouse angiotensinogen gene. 157 74

We investigated the 5'-flanking region of the rat angiotensinogen gene to define the DNA elements conferring inducibility by glucocorticoids and estrogens. Two putative glucocorticoid-responsive elements (GREs) based on sequence comparison were identified. Here we report the functional importance of these sequences. We constructed several deletion mutants of the 5'-region in front of the bacterial reporter gene for chloramphenicol acetyltransferase (CAT). The angiotensinogen-CAT-reporter plasmids (pRagCAT) were transiently transfected into the rat hepatoma cells FTO 2B and Fe 33. All pRagCAT constructs in which the 5'-region contained at least one of the two GRE consensus sequences were stimulated by dexamethasone. On the other hand, deletion mutants containing no GRE sequences were not inducible with dexamethasone. In additional experiments, the transcriptional functions of the two putative GREs were assessed by cloning synthetic oligonucleotides encompassing the GRE sequences directly in front of the heterologous herpes simplex virus thymidine-kinase promoter. Our results showed that each synthetic GRE was capable of stimulating the heterologous TK promoter after administration of dexamethasone and that both GREs together act synergistically. We also investigated the transcriptional control of angiotensinogen by estrogen. Although no estrogen-responsive element consensus sequences were detectable by sequence comparison, we did identify sequences between -60 to -92 which conferred estrogen inducibility to the rat angiotensinogen gene. In this region, a so-called half-palindromic estrogen-responsive element is localized at nucleotides -87 to -91.
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PMID:Glucocorticoid- and estrogen-responsive elements in the 5'-flanking region of the rat angiotensinogen gene. 166 57

We have isolated the human angiotensinogen gene from a genomic library and determined the exon-intron junction sequences. The gene is 12 kilobases long and consists of five exons interrupted by four introns, as a single copy in the human genome. Of particular interest are the positions of the introns in the human angiotensinogen gene which are identical to those in the highly homologous human alpha 1-antitrypsin and alpha 1-antichymotrypsin genes, as well as rat and mouse angiotensinogen genes. Northern blot analysis showed that human hepatoma cells (HepG2) produce a large amount of angiotensinogen mRNA but not human glioma cells (T98G). To assay the promoter activity, the 1.3-kilobase genomic fragment containing the 5'-flanking region, first exon, and a part of first intron at positions -1222 to +44 was fused upstream to the chloramphenicol acetyltransferase gene, then transfected into HepG2 and T98G cells. The gene sequence was active only in HepG2 cells, suggesting the presence of a functional promoter. Analysis of deletion mutants demonstrated that the 76-base pairs region from -32 to +44 containing the TATA box and first exon is the minimal promoter, whose activity is as high as that of the SV40 enhancer-promoter. Since the basal expression of the human angiotensinogen gene is much higher in HepG2 than T98G cells, these results may reflect cell-specific differences in the gene transcription.
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PMID:Structure and expression of the human angiotensinogen gene. Identification of a unique and highly active promoter. 169 23

We have constructed pUCSV0cat with low background of chloramphenicol acetyltransferase (CAT) activity and pUCSV3cat (positive control), both containing a SV40 polyadenylation signal 5' to the CAT-coding gene and to the SV40 promoter, respectively. Using this modified pUCSV0cat, we found that human embryonic 293 cells have the ability to activate the promoter of the human renin gene. In addition, we identified the cis-acting sequences responsible for cell-specific expression of the human angiotensinogen gene in its 5'-flanking region.
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PMID:Regulation of human renin and angiotensinogen genes. 180 39

We transiently transfected fusion genes with the 5'-flanking region of the angiotensinogen gene linked to a bacterial chloramphenicol acetyltransferase (CAT) coding sequence as a reporter into opossum kidney (OK) cells. The addition of 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) (10(-3)-10(-7) M) or forskolin (10(-9)-10(-5) M) stimulated the expression of the plasmid pOCAT [angiotensinogen nucleotide (N) -1498/+18] fusion gene in OK cells in a dose-dependent manner. The addition of dexamethasone (Dex) (10(-6) M) further enhanced the stimulatory effect of 8-BrcAMP or forskolin, whereas the addition of (R)-p-adenosine 3',5'-cyclic monophosphorothioate [(Rp)-cAMP[S], an inhibitor of cAMP-dependent protein kinase A, I and II] blocked the stimulatory effect of 8-BrcAMP. Furthermore, the addition of 8-BrcAMP (10(-3) M) or Dex (10(-6) M) or a combination of both stimulated the expression of pOCAT (angiotensinogen N -1138/+18), pOCAT (angiotensinogen N -960/+18), pOCAT (angiotensinogen N -814/+18), and pOCAT (angiotensinogen N -688/+18), but had no effect on the expression of pOCAT (angiotensinogen N -280/+18), pOCAT (angiotensinogen N -198/+18), pOCAT (angiotensinogen N -110/+18), pOCAT (angiotensinogen N -53/+18), and pOCAT (angiotensinogen N -35/+18). To further localize the putative cAMP-responsive element (CRE) in the angiotensinogen gene, we constructed fusion genes by inserting the DNA fragments angiotensinogen N -814 to N -689, angiotensinogen N -814 to N -761, and angiotensinogen N -760 to N -689 of the 5'-flanking region of the angiotensinogen gene upstream of the thymidine kinase (TK) promoter fused to a CAT gene and introduced them into OK cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of the angiotensinogen gene is synergistically stimulated by 8-BrcAMP and Dex in opossum kidney cells. 784 Mar 9

We have previously reported that addition of 8-bromocyclic AMP enhances the stimulatory effect of dexamethasone on the expression of the angiotensinogen gene in mouse hepatoma cells in vitro. Isoproterenol is known to stimulate the synthesis of hepatic intracellular cyclic AMP via beta-adrenergic receptors. To study the possible effect of beta-adrenergic receptors on the expression of the angiotensinogen gene in mouse hepatoma cells, we transiently transfected them with a fusion gene with the 5'-flanking region of the angiotensinogen gene linked to a bacterial chloramphenicol acetyltransferase coding sequence as a reporter, pOCAT (ANG N-1498/+18). The addition of isoproterenol (10(-9) to 10(-5) mol/L) alone had no stimulatory effect on the expression of pOCAT (ANG N-1498/+18). In the presence of dexamethasone (10(-6) mol/L), however, isoproterenol enhanced the stimulatory effect on the dexamethasone on the expression of pOCAT (ANG N-1498/+18). The enhancing effect of isoproterenol was inhibited by the presence of propranolol (beta 1- and beta 2-adrenergic receptor antagonist) and ICI 118,551 (beta 2-adrenergic receptor antagonist) but not by the presence of atenolol (beta 1-adrenergic receptor antagonist). Furthermore, the addition of Rp-cAMP (an inhibitor of protein kinase A I and II) blocked the enhancing effect of isoproterenol. These studies demonstrated that isoproterenol enhances the stimulatory effect of dexamethasone on the expression of the angiotensinogen gene in mouse hepatoma cells via beta 2-adrenergic receptor and cyclic AMP-dependent protein kinase pathways. Our data may be important in understanding the molecular mechanism(s) of the stimulatory effect of catecholamines/glucocorticoid-induced expression of the angiotensinogen gene in the liver.
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PMID:Beta-adrenergic receptors and angiotensinogen gene expression in mouse hepatoma cells in vitro. 784 40

We previously demonstrated that the 3.8-kilobase DNA fragment containing exons 4 and 5 of the human angiotensinogen (hAG) gene enhances the expression of chloramphenicol acetyltransferase gene, under control of the hAG promoter, in human hepatoma HepG2 cells. In the present study, to define regulatory elements of the hAG gene, we have functionally dissected this downstream region and localized a cell type-dependent enhancer to the 832-base pair sequence containing the exon 5 and 3'-flanking region. Further deletion analyses revealed that the 24-base pair core DNA fragment present in the 3'-flanking region was responsible for this enhancement. Electrophoretic mobility shift assay demonstrated that the 3'-enhancer core element interacts specifically with two nuclear factors from the HepG2 cells, one of which is an uncharacterized factor (human angiotensinogen enhancer factor-1: hAEF-1), the other is an AP-3-related factor. Mutation analyses indicated that the disruption of hAEF-1 binding alone completely impaired the enhancer activity of the core element. These results suggested that the downstream enhancer core element interacting with hAEF-1 plays an important role in activating the angiotensinogen promoter in a cell type-dependent manner.
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PMID:Identification of cell type-dependent enhancer core element located in the 3'-downstream region of the human angiotensinogen gene. 796 7

The catalytic reaction of renin, an aspartyl proteinase, with angiotensinogen is the rate-limiting step fo the renin-angiotensin system involved in the maintenance of blood pressure and electrolyte balance in mammals. We have characterized species-specific expression of the hepatic renin gene by RNase protection experiment, primer extension analysis, and promoter assay using an in vitro DNA transfection. RNase protection experiments revealed that the renin gene is expressed in rat liver, but neither in mouse nor in human. Primer extension analysis identified the putative promoter region of the rat renin gene, which contains TATAAAA sequence, a canonical regulatory DNA element. In order to test whether the upstream region of the renin gene with respect to the putative transcription initiation site is a functional promoter, we have examined the ability of the 5'-flanking sequences of the rat renin gene as well as the human and mouse genes to activate expression of a reporter gene containing the bacterial chloramphenicol acetyltransferase (CAT)-coding sequences, by transient transfection assays. In transfected HepG2 cells, a hepatoma cell line, only the rat renin promoter was capable of driving the CAT gene expression. These results suggested that the rat-specific renin gene expression in the liver could be primarily determined by its promoter specificity.
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PMID:Species-specific expression of the hepatic renin gene. 820 34

Angiotensinogen is abundantly expressed in adipose tissue as well as in liver where it is mainly produced. To address the mechanism of this adipogenic expression, promoter regions of the mouse angiotensinogen gene are fused to the chloramphenicol acetyltransferase reporter gene and stably transfected into 3T3-L1 preadipocytes. Promoter activity correlates well with an increase of mRNA levels during adipogenic differentiation, thereby demonstrating that the induction is primarily due to transcriptional activation. Deletion analysis indicates that the proximal promoter region from -96 to +22 is able to mediate the chloramphenicol acetyltransferase induction and identifies two transcriptionally active regions: AGE1 (position -399 to -139) and AGE2 (position -96 to -52). Heterologous promoter assay reveals that AGE1 behaves with a constitutive enhancer-like property and that AGE2 functions as a differentiation-inducible activator. Gel shift experiments show that AGE2 specifically binds a novel factor (AGF2), which is induced upon differentiation. Furthermore, a constitutive factor (AGF3) binds to the core promoter region including the exon 1 (from -6 to +22, AGE3). Mutations within either AGE2 or AGE3 that disrupt nuclear factors binding in vitro dramatically reduced the chloramphenicol acetyltransferase activation in the native promoter context. These results suggest that both AGE2 and AGE3 are necessary for mediating efficient activation of the mouse angiotensinogen promoter during adipogenic differentiation.
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PMID:Proximal and core DNA elements are required for efficient angiotensinogen promoter activation during adipogenic differentiation. 832 78

We previously identified various upstream and downstream regulatory elements and factors important for hepatic expression of the human angiotensinogen (ANG) gene, the precursor of vasoactive octapeptide angiotensin II. In the present study, to further investigate the molecular mechanism of human ANG transcriptional regulation, we generated transgenic mice carrying the fusion gene composed of the 1. 3-kilobase promoter of the human ANG gene, its downstream enhancer, and the chloramphenicol acetyltransferase reporter gene. Because expression of the chloramphenicol acetyltransferase gene was observed strongly in the liver and weakly in the kidney, we suspected that hepatocyte nuclear factor (HNF) 4 with a tissue expression pattern similar to that of the reporter gene would regulate ANG transcription. In vitro assays indicated that HNF4 bound to the promoter elements and strongly activated the ANG transcription, but that chicken ovalbumin upstream promoter transcription factor (COUP-TF), a transcriptional repressor, dramatically repressed human ANG transcription through the promoter elements and the downstream enhancer core elements. Furthermore, COUP-TF dramatically decreased the human ANG transcription in the mouse liver by the Helios Gene Gun system in vivo. These results suggest that an interplay between HNF4 and COUP-TF could be important in hepatic human ANG transcription.
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PMID:Regulated expression of human angiotensinogen gene by hepatocyte nuclear factor 4 and chicken ovalbumin upstream promoter-transcription factor. 1057 24


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