Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.6 (RNA polymerase)
34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An investigation of the activity of nuclear RNA polymerase following infection of LS cells with HSV-1 shows a decline in both major activities. This effect is not entirely due to inhibition of cellular protein synthesis, and the effect of alpha-amanitin-sensitive RNA polymerase is mediated by a protein(s) synthesized in the infected cell. Changes in the properties of this RNA polymerase activity include a reduction in the relative UTP/GTP incorporation ratio and an increased sensitivity to inhibition by actinomycin D, indicating that RNA polymerase II is involved in virus transcription.
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PMID:The effects of herpes simplex virus type 1 on cellular DNA-dependent RNA polymerase activities. 18 22

Many factors influence the production of 1,25(OH)2D3 (1,25-dihydroxycholecalciferol) by the kidney. One important factor seems to be feedback regulation by 1,25(OH)2D3 itself. Administration of 1,25(OH)2D3 to vitamin D-deficient chicks abolishes renal 25(OH)D3(25-hydroxycholecalciferol)1-hydroxylase activity and induces the appearance of 25(OH)D3 24-hydroxylase activity. It is likely that these effects are mediated via a nuclear effect, as they are prevented by pretreatment with actinomycin D and alpha-amanitin. Further, 1,25(OH)2D3 has a marked effect on gene transcription in the kidney cell, as assessed by measurement of RNA polymerase activities. RNA polymerase I and II activities are 80-90% inhibited by 12.5nmol of 1,25(OH)2D3 within 30min of subcutaneous administration, indicating an immediate and massive decrease in total gene transcription. By 4h RNA polymerase II activity has returned to control values, but RNA polymerase I activity is markedly enhanced. These results are consistent with the view that regulation of cholecalciferol metabolism in the kidney is associated with an effect of the active metabolite on the kidney nucleus.
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PMID:Feedback regulation of vitamin D metabolism by 1,25-dihydroxycholecalciferol. 19 83

We have previously described the isolation, from nuclei of monkey cells infected with Simian virus 40 (SV40), of a nucleoprotein complex which is able to achieve viral transcription. This complex contains SV40 DNA and RNA polymerase II molecules which have initiated transcription during the viral development. We show here, by molecular hybridization experiments, that most of the templates active in SV40 transcription can be dissociated from host DNA. In conditions where supercoiled SV40 DNA form I sediments at 21 S, the transcription complex has a sedimentation coefficient of about 25 S. Inhibition of viral DNA synthesis by cytosine arabinonucleoside or chloroquine does not affect the activity of the transcription complex, which suggests that replicating molecules are not required for viral RNA synthesis and that SV40 DNA form I could serve as template for late SV40 transcription. A large fraction of the RNA synthesized in vitro remains associated with the SV40 DNA template in cesium sulfate density gradient. The RNA chains produced by the complex are heterogeneous in size, most of them being as large or larger than the viral genome.
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PMID:Characterization of a soluble simian-virus-40 transcription complex. 19 51

Cellular RNA synthesis was studied in mouse L-929 cells and in these cells infected with mengovirus. RNA polymerases I, II, and III were partially purified and their chromatographic properties were analyzed by DEAE-Sephadex A-25 chromatography. RNA polymerase II was purified from mouse liver and its subunit structure was compared to that of normal and virus-infected L-929 cells by two-dimensional gel electrophoresis. By these criteria, the enzymes from all three sources were identical. The RNA synthetic activities and capacities of chromatins from normal and virus-infected cells were compared under a variety of conditions. The endogenous activity in chromatin from infected cells was inhibited relative to controls but the residual activity responded normally to stimulation by ammonium sulfate, heparin, and Sarkosyl. The template capacity of the chromatins was compared with added RNA polymerase II and by a rifampicin challenge assay utilizing Escherichia coli RNA polymerase. Identical results were obtained in each case. The number of growing RNA chains and the rates of their elongations were determined. The results showed that nuclei and chromatin from infected cells have a smaller number of RNA polymerase II molecules engaged in RNA synthesis than normal cells do but that the active molecules elongate RNA chains at the same rate.
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PMID:Cellular RNA synthesis in normal and mengovirus-infected L-929 cells. 20 39

The effect of low concentrations of cyclic GMP (guanosine 3':5'-cyclic monophosphate) on the in vitro enzymatic activities of DNA-dependent RNA polymerases isolated from human peripheral blood lymphocytes has been investigated. In agreement with earlier studies which employed isolated nuclei as the enzyme source, an increase in the activity of partially purified RNA polymerase I is observed in the presence of cyclic GMP (10(-8) to 10(-10)M). RNA polymerase II activity is inhibited by the presence of cyclic GMP at concentrations between 10(-4) and 10(-10)M. RNA polymerase III activity is stimulated in a bimodal fashion by the presence of cyclic GMP with maximal activity noted at 10(-8) to 10(-10) M and 10(-5)M. In addition, [3H]cyclic GMP binds specifically to chromatographic fractions which are known to contain RNA polymerases I, II and III. This binding to RNA polymerases II and III is apprarently less tenacious as demonstrated by dissociation studies. The observations provide additional evidence for a role for cyclic GMP in the regulation of RNA synthesis.
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PMID:Modification of human DNA-dependent RNA polymerase activity by cyclic GMP. 20 24

SV40 chromatin obtained from infected monkey cells was used to study the effect of the viral chromatin proteins on endogenous RNA polymerase II. Ammonium sulfate activated the rate of transcription by endogenous RNA polymerase in two ways: 1) by direct action on the enzyme; and 2) by causing a reversible conformational change in the viral chromatin. Under optimal reaction conditions, the viral chromatin proteins did not limit the rate of RNA chain elongation, and high molecular weight RNA (1.6 X 10(6) d) was synthesized by the SV40 chromatin.
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PMID:The sv40 transcription complex. I. Effect of viral chromatin proteins on endogenous RNA polymerase activity. 20 28

Nucleoplasmic RNA polymerase II (nucleosidetriphosphate:RNA nucleotidyltransferase, EC 2.7.7.6) from calfthymus is phosphorylated by homologous cyclic AMP-independent protein kinase (ATP:protein phosphotransferase, EC 2.7.1.37). Polyacrylamide gel electrophoresis of the 32P-labeled RNA polymerase II under non-denaturing conditions revealed that both forms of the enzyme were phosphorylated. Polyacrylamide gel electrophoresis of the 32P-labeled RNA polymerase II under denaturing conditions showed that the 25 000 dalton subunit was the phosphate acceptor subunit. Partial acid hydrolysis of the 32P-labeled RNA polymerase II followed by ion-exchange chromatography revealed serine and threonine as the [32P]phosphate acceptor amino acids. Phosphorylation of the RNA polymerase II was accompanied by a stimulation of enzymatic activity and was dependent upon the presence of ATP.
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PMID:Phosphorylation of calf thymus RNA polymerase II by nuclear cyclic 3',5'-AMP-independent protein kinase. 20 18

Mouse two-cell embryos, morulae, and blastocysts were killed when infected in vitro with simian virus 40 (SV40) at high multiplicities of infection. Polyoma virus was not deleterious for preimplantation embryos, even at a very high multiplicity of infection; however, the outgrowths of polyoma-infected blastocysts disintegrated after several days of culture. Indirect immunofluorescence tests revealed the presence of SV40 T and V antigens and polyoma virus V antigen in the nuclei of trophoblastic cells. Virus-specific antigens were not found in the nuclei of cells forming inner cell masses of blastocysts or in inner cell mass-derived cells in blastocyst out-growths. The appearance of SV40 T and V antigens in the nuclei was inhibited by alphaamanitin, a RNA polymerase II inhibitor. The amount of infectious virus recovered from cultures of morulae or blastocysts on subsequent days after infection with SV40 initially declined but later increased. These points of evidence indicate that some cells of early mouse embryos are permissive for the expression of early and late functions of SV40 genome and that susceptibility to infection with polyoma virus and/or permissiveness for the expression of polyoma virus late functions develop gradually between the two-cell and blastocyst stages. Electron microscope observations showed the presence of specific complexes of membranes and virions in the cytoplasm of trophoblastic cells. Single viral particles could be found in the nuclei and also in mitochondria.
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PMID:Infection of mouse preimplantation embryos with simian virus 40 and polyoma virus. 20 44

Glucocorticoid hormone treatment of GR cells, a cultured line derived from mouse mammary tumor tissue, selectively stimulates the rate of transcription of integrated proviral genes specifying mammary tumor virus (MTV). We have incubated isolated nuclei from these cells under conditions in which all three endogenous RNA polymerases appear to be active. RNA synthesized in vitro is distinguished from preexisting nuclear RNA by labeling the in vitro products with [3H]CTP, and the level of MTV RNA synthesis is measured by molecular hybridization with unlabeled viral DNA. Synthesis requires the addition of nucleoside triphosphates, and is inhibited by actinomycin D. Pretreatment of GR cells with dexamethasone, a synthetic glucocorticoid, has no significant effect on the amount of total RNA synthesis in isolated nuclei. In contrast, synthesis of MTR RNA is stimulated 10-20-fold in nuclei from dexamethasone-treated cells relative to untreated control nuclei; the sensitivity of in vitro viral RNA synthesis to inhibition by alpha-amanitin suggests that it is carried out exclusively by RNA polymerase II. The fraction of total RNA synthesis which is viral specific (about 0.2-0.4% in nuclei from dexamethasone-treated cells and 0.01-0.03% in controls) is similar to that detected in pulse labeled RNA from whole GR cells in culture. Our procedures for labeling and hybridization of RNA appear to avoid artifacts recently noted in other in vitro transcription systems.
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PMID:Synthesis of mouse mammary tumor virus ribonucleic acid in isolated nuclei from cultured mammary tumor cells. 20 79

The mechanism of the priming effect of luteinizing hormone releasing factor (LH-RF) upon gonadotrophin secretion was studied using short-term incubation of hemipituitary glands from pro-oestrous rats. The dependence of the priming, but not the LH releasing action of LH-RF on protein synthesis in pituitary tissue was confirmed. Cytochalasin B failed to affect the first response to LH-RF, but abolished the priming effect, suggesting that the integrity of cellular microfilaments was essential. Colchicine and vinblastine did not modify the response to LH-RF. Neither inhibitors of DNA nor the inhibitor of RNA polymerase II, alpha-amanitin, significantly affected the priming action of LH-RF. Normal extracellular concentrations of Ca2+ were necessary for gonadotrophin release, but the priming effect was not significantly affected by low extracellular Ca2+ and could not be elicited by raising intracellular Ca2+ concentrations. Adenosine 3':5'-cyclic phosphate did not appear to act as a second messenger for either the gonadotrophin releasing or the priming action of LH-RF.
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PMID:Priming effect of luteinizing hormone releasing factor in vitro: role of protein synthesis, contractile elements, Ca2+ and cyclic AMP. 22 30


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