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:2.7.7.6 (RNA polymerase)
34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were made on the effects of alpha-amanitin, cycloheximide, and thioacetamide on synthesis and content of low molecular weight nuclear RNA. Cycloheximide, an inhibitor of protein synthesis and the synthesis of 45S pre-rRNA and 5S RNA, also inhibited synthesis of nuclear U1 and U3 RNAs. alpha-Amanitin, an inhibited the synthesis of U1 and U2 low molecular weight nuclear RNA. Thioacetamide, which induces nucleolar hypertrophy and increased nucleolar RNA polymerase activity, markedly increased synthesis of 5.8S RNA and U3 RNA. These results show that syntheses of individual low molecular weight nuclear (LMWN) RNAs are controlled by different regulatory mechanisms. In particular, there appears to be a specific relationship between U3 RNA and functional states of the nucleolus.
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PMID:Effects of alpha-amanitin, cycloheximide, and thioacetamide on low molecular weight nuclear RNA. 18 18

Treatment of rat thymus cells with the glucocorticoids cortisol and dexamethasone resulted in the stimulation of RNA polymerase B activity within 10 min of steroid addition. This early effect was followed by the inhibition of both RNA polymerase A and B activities. These effects were glucocorticoid-specific and were inhibited by the antiglucocorticoid cortexolone. The inhibitory effect of dexamethasone on RNA polymerase A activity was abolished by prior treatment of the cells with alpha-amanitin, cordycepin or cycloheximide, but cycloheximide was only capable of inhibiting the steroid effect measured at 3 h if added within 10--20 min after steroid addition. Cycloheximide had no effect on the steroid-mediated inhibition of RNA polymerase B activity. Control RNA polymerase A activities were unaffected by the presence of inhibitors of RNA and protein synthesis. It is concluded that the inhibition of ribosomal RNA synthesis by glucocorticoids is dependent on protein synthesis, but that basal RNA polymerase A activity in rat thymus cells is not stringently coupled to protein synthesis.
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PMID:Glucocorticoid regulation of rat thymus RNA polymerase activity: the role of RNA and protein synthesis. 30 18

Rat liver RNA polymerase I solubilized from isolated nuclei and present in a soluble form in the cytoplasmic fraction has been analyzed by phosphocellulose chromatography 3 hours after the administration of cycloheximide. The antibiotic did not induce any change in the chromatographic properties of both nuclear and cytoplasmic RNA polymerase I. They appeared to remain in the IB and IA forms, characteristic of the transcribing (IB) and non-transscribing (IA) enzyme. While the level of the nuclear enzyme was not modified, the level of the cytoplasmic one appeared significantly increased. These results support previous ones indicating that the cycloheximide-induced inhibition of ribosomal RNA synthesis cannot be merely explained by a decrease in the nuclear or cellular level of RNA polymerase I. The cellular level of RNA polymerase I, taking into account the relative proportion of the enzyme found in nuclei and cytoplasm, appeared to be slightly increased. Cycloheximide administration did not seem to result in the appearance, in intact nuclei, of enzyme molecules in a free form or as blocked transcription complexes. It is concluded that the antibiotic affects the catalytic efficiency rather than the number of RNA polymerase I molecules actually engaged in the transcription of ribosomal cistrone.
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PMID:[Reduced catalytic effectiveness of RNA polymerase I in hepatocytes of rats treated with cycloheximide]. 54 55

The administration of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) to rachitic chicks produces an increase in (a) RNA and protein synthesis, (b) calcium binding protein (CaBP) concentration, and (c) alkaline phosphatase activity in the duodenum. These events occur concomitantly with enhanced calcium transport. We inhibited RNA and protein synthesis in richitic chicks and measured the subsequent response to 1,25(OH)2D3. Actinomycin D, injected prior to and following 1,25(OH)2D3 administration, inhibited intestinal RNA polymerase activity, blocked the rise in serum calcium, reduced the amount of CaBP, and increased alkaline phosphatase activity. Cycloheximide injected in similar fashion, inhibited the 1,25(OH)2D3-mediated increase in intestinal protein synthesis, serum calcium, CaBP, and alkaline phosphatase activity. Neither inhibitor blocked the ability of 1,25(OH)2D3 to stimulate calcium transport as measured in isolated duodenal loops in vivo. The ability of either inhibitor to block 1,25(OH)2D3-mediated calcium transport despite inhibition of CaBP production and alkaline phosphatase activity (by cycloheximide) indicates that de novo RNA and protein synthesis, and in particular CaBP and alkaline phosphatase, are not required for the 1,25(OH)2D3 stimulation of calcium transport.
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PMID:Independence of 1,25-dihydroxyvitamin D3-mediated calcium transport from de novo RNA and protein synthesis. 61 81

The addition of cycloheximide to a thermosensitive conditional yeast mutant (ts-187) before and after transfer to the nonpermissive temperature (36 degrees C) for initiation of protein synthesis produces the uncoupling of the RNA and protein synthetic machineries. Since the drug can produce this relaxation in the presence and absence of protein synthesis, it is concluded that the coupling of protein and RNA synthesis, which a temperature shift produces, is not exclusively related to the inhibition of protein synthesis. Support for this assumption has been obtained using the parental (A364A) strain. Transferring this strain to 36 degrees C produces inhibition of RNA synthesis in the presence of stimulation of protein synthesis. Furthermore, cycloheximide and edeine prevent this inhibtion of RNA synthesis that temperature shift produces. It is, therefore, postulated that this inhibition of RNA synthesis results from the synthesis or activation of a factor(s) elicited by the increase in temperature whose function is to repress the transcriptional apparatus. Cycloheximide or edeine can prevent the function of this repressor-like factor by binding to the factor or by preventing its synthesis. The fact that inhibition of protein synthesis either by cycloheximide action or temperature shift in ts-187 produces inhibition of RNA synthesis in isolated nuclei indicates that, in addition to the aforementioned repressor, other factor(s) having a promoter function may exist. Since a slight inhibition of protein synthesis produces nuclear template restrictions, it is postulated that the promoter-like factor(s) is a polypeptide different from the RNA polymerase and, at least in yeast, has a high turnover.
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PMID:Control of ribonucleic acid synthesis in eukaryotes. 3. The effect of cycloheximide and edeine on rna synthesis in yeast. 77 14

Nuclear RNA polymerase activity was studied in homotransplanted rat glial tumors where the primary tumor was produced by transplacental injection of ethylnitrosourea. Alpha amanitin, cycloheximide, and rifampicin were tested as inhibitors of this activity. Alpha amanitin significantly inhibited RNA polymerase activity in all tumors. This indicated that the major nuclear RNA polymerase activity seen in vitro in the tumor nuclei was RNA polymerase II. This is similar to the activity seen in normal glial nuclei. Cycloheximide and rifampicin which have no effect on RNA polymerase activity in normal glial nuclei inhibited about 20% of the polymerase activity in three of the tumors. The size and multiplicity of the nucleoli in these tumor cells suggests that RNA polymerase I could account for the activity which is inhibited by cycloheximide.
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PMID:RNA polymerase activity in homotransplanted rat brain tumors initially induced by ethylnitrosourea. 114 4

alpha-Amanitin, an inhibitor of RNA polymerase II, has little effect on either UV-induced incision or repair synthesis in cultured normal human fibroblasts but almost completely inhibits both processes in xeroderma pigmentosum group C fibroblasts. Cycloheximide, at a concentration which inhibits protein synthesis by 75-80%, has no effect on incision or repair synthesis in either cell type, which argues that the effects of alpha-amanitin on repair occur at the level of transcription. Cot analysis demonstrates that UV-induced repair synthesis occurs at similar levels in highly repetitive, middle repetitive and single copy sequence in both normal and xeroderma group C cells. We conclude that normal cells must have at least two excision repair pathways for repair of UV-induced damage, one dependent on transcription and the other independent.
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PMID:Transcription-dependent and independent DNA excision repair pathways in human cells. 137 32

Cycloheximide generally inhibits steroidogenesis, but has different effects on the accumulation of the mRNAs for various steroidogenic enzymes in different species, tissues, and cell lines. In bovine adrenocortical cells, cycloheximide prevents ACTH- or cAMP-induced accumulation of the mRNAs for cytochrome P450scc and adrenodoxin, but in human cells, cycloheximide induces the accumulation of adrenodoxin mRNA. To study the potential role of the 3'-untranslated regions, and especially the AU-rich regions, of adrenodoxin and P450scc mRNAs in cycloheximide-sensitive regulation of mRNA accumulation, we constructed a series of vectors expressing P450scc or adrenodoxin mRNA with its own or each other's 3'-untranslated sequences and transfected them into human JEG-3 cytotrophoblast cells. Removal of the AU-rich 3'-untranslated sequences of adrenodoxin mRNA and replacing them with the 3'-untranslated region of P450scc did not alter the abundance or apparent stability of this mRNA, or its inducibility by cycloheximide or cAMP. Substituting the AU-rich 3'-untranslated region of adrenodoxin mRNA (which contains three copies of the AUUUA sequence) for the 3'-untranslated region of P450scc did not alter the inducibility of P450scc mRNA with forskolin. Inhibition of transcription with actinomycin-D elicited no difference in the adrenodoxin mRNA half-life in JEG-3 cells treated with forskolin, cycloheximide, or both. RNA polymerase run-on assays show little effect of forskolin on adrenodoxin gene transcription, while P450scc gene transcription was induced. These data suggest that the principal means for regulating P450scc mRNA is transcriptional, while the principal regulation of adrenodoxin is posttranscriptional. This posttranscriptional regulation of adrenodoxin mRNA is not mediated by the AUUUA sequences or other segments of the 3'-untranslated region.
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PMID:Regulation of human cytochrome P450scc and adrenodoxin messenger ribonucleic acids in JEG-3 cytotrophoblast cells. 144 36

Effects of dexamethasone, EGF and insulin on the synthesis of rRNA and phosphorylation of nucleolin in primary cultures of adult rat hepatocytes were studied. Hepatocytes were incubated for 8 h with EGF (20 ng/ml) plus insulin (0.1 microM) and/or for 20 h with dexamethasone (1 microM) before the end of incubation. The incorporation of [3H]uridine into acid-insoluble materials and the nuclear activity of RNA polymerase I were stimulated approx. 2-fold with EGF plus insulin and these were further enhanced 2-3-times by dexamethasone, although dexamethasone alone exerted no stimulation. When hepatocytes were incubated with [32P]orthophosphate, similar enhancement by these hormones was also observed in the phosphorylation of a nucleolar protein, nucleolin, which was detected by immunoprecipitation with anti-nucleolin antibodies. The amount of nucleolin was slightly increased by EGF plus insulin in the presence of dexamethasone, but scarcely changed by treatment with EGF plus insulin or dexamethasone alone. Cycloheximide inhibited RNA synthesis to a greater or lesser degree in the case of all hepatocytes which were cultured with or without these hormonal treatments. These results indicate that the in vivo effect of glucocorticoid on rRNA synthesis and nucleolin phosphorylation in liver is primarily a direct action on parenchymal cells and requires other growth factors such as EGF and insulin.
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PMID:Synergistic stimulatory effect of glucocorticoid, EGF and insulin on the synthesis of ribosomal RNA and phosphorylation of nucleolin in primary cultured rat hepatocytes. 171 Sep 32

Cycloheximide (Cyh), administered at a dose of 5 mg/kg body wt blocks protein synthesis in normal rat liver (NRL) and regenerating rat liver (RRL). The rate of synthesis of 45S pre-rRNA in RRL, studied after RNA labelling in vivo is activated 2.8 times. Pre-r RNA synthesis in RRL is more sensitive to the stopped translation, but never falls down to the level in NRL. The major contribution to the rDNA transcription activation in RRL comes from the 20-fold increase in the number of pol I molecules engaged in the transcription, the elongation rate being 1.4-fold accelerated. Cyh quenches partially the enhanced rDNA transcription in RRL: the number of pol I molecules and their elongation rate are about 1.7-fold and 1.5-fold higher, respectively, than the corresponding values in NRL after Cyh treatment. The results show that two different mechanisms control the number and the rate of initiation and elongation of RNA polymerase I in rat liver; one of them depends on continuous protein synthesis and can be inactivated by Cyh, the other is Cyh resistant.
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PMID:Activated ribosomal RNA synthesis in regenerated rat liver upon inhibition of protein synthesis. 187 19


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