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)

The present study describes the separation and purification of a reverse transciptiase from an orbital tumor of a patient with acute myelomonocytic leukemia. Specific reaction conditions with respect to ionic requirements and template-primers are reported. The purified enzyme was able to transcribe (rA)n . (dT)12, (rC)n . (dG)12, (OMeC)n . (dg)12 and the 70 S RNA from R(Mu)LV. Serological studies that the reverase transcriptase is antigenically related to reverse transcriptase from the type C woolly monkey virus-gibbon ape leukemia virus group.
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PMID:RNA-dependent DNA polymerase activity in ocular granulocytic sarcoma associated to acute myelomonocytic leukemia in Turkish children. Biochemical and immunological characterization of the enzyme. 615 28

A factor stimulating RNA polymerase II purified from Ehrlich ascites tumor cells was found to stimulate alpha-amanitin-sensitive RNA synthesis in nuclei isolated from spleen cells of anemic mice, though less than it stimulated purified RNA polymerase II. The fidelity of the resulting RNA synthesis was monitored by measuring the stimulation of globin mRNA synthesis. Globin mRNA was measured quantitatively by DNA-RNA hybridization by using plasmid DNA containing globin DNA sequences. Results showed that the synthesis of globin mRNA was enhanced in isolated nuclei in the presence of this factor coinciding with an increase of overall alpha-amanitin-sensitive RNA synthesis. Thus, it was concluded that an externally added factor did not stimulate random transcription but meaningful RNA synthesis in isolated nuclei.
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PMID:Stimulation of messenger ribonucleic acid synthesis in isolated nuclei by a protein that stimulates RNA polymerase II. 616 47

The incubation of Krebs ascites tumor cells in medium with a high salt concentration resulted in a partial inhibition of nuclear RNA synthesis. The residual RNA polymerase activity in such nuclei was only slightly inhibited by low concentrations (50 nM) of alpha-amanitin. This finding suggested an inhibition of RNA polymerase II activity under conditions of medium hypertonicity. Indeed, RNA polymerase II, isolated from the nuclei of cells exposed to hypertonicity, revealed only half of the control activity. On the other hand, RNA polymerase I was not affected by hypertonicity. Moreover, chromatin fractions isolated from cells incubated in hypertonic or isotonic medium were equally template-active in RNA synthesis.
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PMID:High salt effect on RNA synthesis in Krebs ascites tumor cells. 617 84

A novel enzyme inhibitor against RNA-directed DNA polymerase of avian myeloblastosis virus was produced by an isolate of a new streptomycete for which the name Streptomyces retrostaticus is proposed. This enzyme inhibitor, which was named retrostatin, did not inhibit DNA-directed DNA polymerase of Escherichia coli and DNA-directed RNA polymerase of Ehrlich ascites tumor cells. Retrostatin was produced by the microorganism together with streptonigrin. These two substances were extracted from the culture broth with ethyl acetate at acidic pH. Retrostatin is an acidic pH indicator and the free acid was recovered as a red powder. Retrostatin had weak antibiotic activities against Gram-positive bacteria and yeasts.
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PMID:Retrostatin, a new specific enzyme inhibitor against avian myeloblastosis virus reverse transcriptase. 619 91

The effect of mitoxantrone on the template activity of nuclei isolated from the T-47D human breast tumor cell line was investigated. The results suggest that mitoxantrone significantly inhibits total RNA synthesis of these nuclei in a concentration-dependent manner. At low drug concentrations (10(-9) M and 10(-7) M) RNA synthesis was inhibited by 21.9% and 41% compared to control values, respectively. Greater inhibition was observed when the mitoxantrone concentration was increased to 10(-5) M or 10(-4) M (56% and 77%, respectively). Experiments utilizing alpha-amanitin revealed that mitoxantrone inhibits RNA polymerase II activity in a concentration-dependent manner.
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PMID:Acute effects of mitoxantrone on the template activity of isolated nuclei from the T-47D human breast tumor cell line. 619 72

We have isolated a unique 35 base pair region of avian tumor virus DNA that binds specifically to Escherichia coli RNA polymerase holoenzyme. Studies with various size classes of viral DNA coupled with restriction enzyme mapping data indicate that the binding site is located in the large terminal repeat of the viral genome and is within the first 50 nucleotides of the heteropolymeric region corresponding to the 3'-end of the virion RNA.
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PMID:Binding of Escherichia coli RNA polymerase to a specific site located near the 3'-end of the avaian sarcoma virus genome. 624 69

Cloned DNA templates were used to direct the transcription of early and late simian virus 40 (SV40) genes by a cell-free RNA-synthesizing system. Transcription by RNA polymerase II was sensitive to low levels of alpha-amanitin and completely dependent on exogenously added DNA template. RNA products of discrete lengths were efficiently synthesized when transcription was directed by DNA restriction fragments containing promoter sequences for either early or late genes of SV40. Addition of the D2 tumor antigen to the template DNA inhibited transcription originating from the SV40 early promoter. In contrast, the D2 protein had little or no effect on the transcription from SV40 or adenovirus 2 (Ad2) late promoter sequences. When a mixture of cloned DNA containing SV40 early promoter and Ad2 late promoter was used to direct RNA synthesis, the D2 protein specifically inhibited the synthesis of SV40 early genes but not that of Ad2 late sequences. The D2 DNA binding protein also had no effect on the transcription directed by SV40 mutant templates that contain an intact early promoter sequence but lack specific tumor-antigen binding sites. We have confirmed that, under the conditions of the transcription assay, the D2 protein binds and interacts specifically with its recognition sites on wild-type template DNAs but fails to bind to mutant or Ad2 DNA templates that lack sequences containing SV40 tumor-antigen binding sites. These findings provide evidence that a direct interaction between tumor antigen and its specific binding sites on DNA is the mechanism by which the SV40 A gene autoregulates its transcription.
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PMID:Regulation of simian virus 40 early transcription in vitro by a purified tumor antigen. 625 60

We have placed a 225-bp fragment from the 5' end of the mouse rDNA transcription unit (from -169 to +56) in front of the SV40 tumor antigen coding sequence. After microinjection of this chimeric plasmid into nuclei of mouse L-cells expression of SV40 large T antigen has been observed. The expression of T antigen was dependent on the correct orientation of the rDNA fragment relative to the T antigen-coding region and was seen only in mouse cells. This indicates that the 225-bp rDNA fragment contains the sequence information required for pre-rRNA transcription and demonstrates for the first time that a protein-coding gene can be transcribed and expressed under the control of an RNA polymerase I promoter.
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PMID:Expression of an mRNA coding gene under the control of an RNA polymerase I promoter. 632 Nov 60

We examine the influence of the immunoglobulin locus on the expression of the translocated c-myc oncogene in mouse plasmacytomas. The level of c-myc RNA was 30- 35-fold greater in tumor cells than in normal, quiescent B cells. Mitogen stimulation of the lymphocytes with lipopolysaccharide induced a 15-fold increase in c-myc expression per cell to a level that was similar to that in the transcription of the translocated c-myc gene involved initiation from sequences in the first c-myc intron. Abundant RNA transcripts were also found from the noncoding strand of the c-myc intron in most tumor lines. S1 nuclease mapping was used to locate the intronic sequences that are used to initiate the tumor-specific c-myc RNAs. Six different initiation sites within the intron were mapped, none of which have the TATA sequence usually associated with eucaryotic RNA polymerase II promoters. The noncoding strand transcripts were also found to initiate in the c-myc intron. Transcription of the c-myc coding strand was independent of the position of the translocation breakpoint, even when the heavy chain switch and constant regions were deleted.
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PMID:Transcriptional activation of the translocated c-myc oncogene in mouse plasmacytomas: similar RNA levels in tumor and proliferating normal cells. 632 72

Transcription initiation sites were mapped on both the octopine pTi Ach5 and the nopaline pTI C58 plasmids of Agrobacterium tumefaciens. Transcription ternary complexes were subjected to electrophoresis on agarose gels, prior and/or subsequent to restriction endonuclease digestion of the DNA template, evidenced by autoradiography and located on the restriction maps of the two tumor-inducing plasmids. A. tumefaciens RNA polymerase promptly recognizes and starts transcription on a few sequences which include the T-DNA.
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PMID:Mapping of promoter-proximal regions by in vitro transcription of two Agrobacterium tumefaciens Ti-plasmids. 647 59


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