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)

Small poly(A)-containing RNA molecules which hybridize to the ubiquitous short repetitive sequence B2 and which are transcribed by RNA polymerase III have been identified in the cytoplasm of mouse cells. Here we describe the structure of this small B2 RNA. A cDNA library was prepared from low-molecular weight cytoplasmic poly(A)+RNA isolated from Ehrlich carcinoma cells and the clones which hybridized to B2 sequence were selected. The clones were sequenced and shown to contain B2 sequences followed by a poly(A) tract. The sequences of the cloned B2 RNAs differ from each other by 3-10%, being similar in this respect to genomic B2 copies. Thus, B2 RNA is transcribed from many different B2 sequences in the genome. The 5'-ends of B2 RNA at least in most molecules coincide with the beginning of B2 genomic sequence. The poly(A) segments located at the 3'-end of small B2 RNA are the same size as in mRNA molecules, suggesting posttranscriptional formation. In some clones additional sequences were detected between the 3'-end of B2 sequence and the poly(A) stretch. They seem to result from a lesion in the RNA polymerase III terminator in the corresponding B2 sequences. A model of B2 RNA secondary structure is suggested.
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PMID:[The structure of small polyadenylated B2-RNA]. 380 13

Brain RNA polymerase isolated from rats treated with pemoline and magnesium hydroxide (Cylert) was not more active than enzyme from control animals. The drug did not increase enzymic activity in vitro. Pemoline did not significantly affect either RNA or protein synthesis in suspensions of Ehrlich ascites carcinoma cells.
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PMID:Pemoline and magnesium hydroxide: lack of effect on RNA and protein synthesis. 438 48

8006-I is an antibacterial antibiotic with a rather broad spectrum of activity. The minimum inhibitory concentrations for the most sensitive bacteria are in the range of one to ten micrograms/ml. Yeasts are not affected by concentrations up to 100 micrograms/ml. Some filamentous fungi like Fusarium oxysporum and Mucor miehei are inhibited at 100 micrograms/ml. In Ehrlich carcinoma ascitic cells the incorporation of uridine and leucine and to a lesser extent that of thymidine is reduced. In isolated nuclei of these cells the incorporation of UTP into RNA is inhibited. At low concentrations, the incorporation of uracil into trichloroacetic acid-precipitable material is almost completely inhibited in cells of Bacillus subtilis; at higher concentrations all macromolecular syntheses are affected. No reduction of respiration of the cells is observed. The antibiotic exhibits weak hemolytic activity and lytic activity towards bacteria. In vitro an inhibition of both DNA- and RNA polymerase from Escherichia coli is observed. Poly(U)-directed poly(Phe) synthesis is not affected.
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PMID:8006-I, an antibiotic from Amblyosporium spongiosum (Pers.) Hughes sensu Pirozynski. II. Biological properties. 617 18

Macbecin I showed marked antitumor activity against intraperitoneally (ip) inoculated leukemia P388, melanoma B16, and Ehrlich carcinoma in mice on ip administration. The maximum effect measured in terms of ILS% (increase of life span) was 97 at a daily dose level of 10 mg/kg for leukemia P388, 103 at 5 mg/kg for melanoma B16, and 206 at 10 mg/kg for Ehrlich carcinoma. The effect of macbecin I on leukemia L1210 was slight (39 ILS%) and no activity was observed against leukemia L5178Y or P388/P-3 (a line of P388 resistant to ansamitocin P-3), or MOPC-104E myloma. Three to six hours after administration of 0.5 mg/kg or more of macbecin I to mice bearing ascites leukemia P388 cells, typical karyorrhexis followed by cytolysis in P388 cells was observed. Cytocidal changes induced by macbecin I were also observed in cells which were temporarily prevented from entering mitosis by treatment with known antitumor agents such as 5-fluorouracil, cyclophosphamide, and neocarzinostatin, whereas such cytolysis was not observed in cells which were arrested in metaphase by treatment with ansamitocin P-3. Cytotoxicity of macbecin I to cultured KB cells was observed at doses of 10(-1) micrograms/ml and more. Reverse transcriptase and terminal deoxynucleotidyl transferase activities were not inhibited by macbecin I.
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PMID:Antitumor and cytocidal activities of a newly isolated benzenoid ansamycin, macbecin I. 618 64

From submerged cultures of Lachnella villosa, Lachnella sp. 541, and Peniophora laeta we isolated marasmic acid (1), a metabolite first described from surface cultures of Marasmius conigenus. The sesquiterpenoid exhibits potent antimicrobial and cytotoxic properties. In cells of the ascitic form of Ehrlich carcinoma RNA and DNA syntheses are preferentially inhibited. Marasmic acid inhibits RNA synthesis in isolated nuclei, but does not interfere with the transport of nucleoside precursors into the cells. RNA polymerase II and capping enzyme (mRNA guanylyltransferase), two enzymes of nucleic acid metabolism, are markedly affected after preincubation with marasmic acid. We assume that marasmic acid acts on nucleic acid syntheses by direct inhibition of some of the enzymes involved. This mode of action would also explain its mutagenic properties. The preparation and testing of two derivatives, 2 and 3, revealed that the alpha,beta-unsaturated aldehyde is essential for the antimicrobial and cytotoxic activity of marasmic acid.
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PMID:Antibiotics from basidiomycetes. XVII. The effect of marasmic acid on nucleic acid metabolism. 630 12

In rats bearing a subcutaneously implanted Walker 256 carcinoma an early rise in liver DNA content was followed by a two-fold increase in RNA content between the 6th and 10th day of tumour growth. Total hepatic neutral ribonuclease and its inhibitor were unaffected by tumour growth. No alteration in RNA polymerase I and II activities of liver nuclei was observed except for a 47% increase in RNA polymerase I on the 8th day of tumour growth.
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PMID:Effect of tumour growth on hepatic neutral ribonuclease and its inhibitor and on RNA polymerase activity of liver nuclei. 665 44

By serial transplantation of CS 1, a subline of Shionogi carcinoma SC 115, to female mice, another subline was obtained and designated CS2. The subline showed a complete loss of androgen dependency on the growth of the tumor. When male mice bearing the tumor were castrated and treated with testosterone, the activity of RNA polymerase I in isolated nuclei from the tumor hardly varied during the period of the experiments (36 h), while the activity of RNA polymerase II exhibited a transient increase (about 40%) at 6 h after the testosterone injection. The results, together with the previous ones showing 80% and 40% increases in RNA polymerase I activity at 24 h after testosterone administration in the case of SC 115 (androgen-dependent tumor) and CS 1 (less androgen-dependent tumor), respectively, indicate that the stimulation of RNA polymerase I activity by androgen in the tumor tissues is closely related to the androgen dependency on the growth of the tumors.
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PMID:In vitro effect of androgen on RNA synthesis in nuclei from androgen-independent subline of Shionogi carcinoma (CS 2). 667 65

The present study was undertaken to define the gene(s) of importance on the long arm of chromosome 18 (chromosome 18q) in endometrial carcinomas. We analyzed loss of heterozygosity (LOH) at 3 loci on chromosome 18q and DCC gene expression by the reverse-transcriptase/polymerase chain reaction (RT-PCR) method. Among 61 tumors that were informative, 16 (26%), estimated to be a minimum number, showed allelic losses at one or more chromosome 18q loci. Deletions in these tumors possibly involved the region within or near the chromosome 18q 21.3 band where the DCC gene was localized. Moreover, the incidence of altered DCC mRNA expression was high in these tumors. Appropriate transcription was lost in 5 of 7 (71%) carcinoma cell lines in addition to 14 of 28 (50%) surgically resected tumors. Histopathological differentiation and clinical stage of disease were not related to LOH frequency or to DCC mRNA expression. These results suggest that the target for allelic loss on chromosome 18q seen in endometrial carcinomas is the DCC gene, and that inactivation of this gene may be critical for the development of most endometrial carcinomas.
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PMID:DCC gene alteration in human endometrial carcinomas. 751 50

The genes CDKN2B (MTS2) and CDKN2 (MTS1) encoding the proteins p15 and p16 are both located on chromosomal band 9p21, a locus at which frequent homozygous and heterozygous deletions occur in many primary human tumors, including esophageal carcinoma. CDKN2 and CDKN2B belong to a family of cyclin-dependent kinase 4 inhibitors (INK41) and control cell proliferation during the G1 phase of the cell cycle. Their inactivation may contribute to uncontrolled growth in human cancers. To investigate whether CDKN2B and CDKN2 are involved in esophageal tumorigenesis, we studied homozygous deletion, intragenic mutation, and messenger RNA (mRNA) expression of CDKN2 and CDKN2B in nine esophageal squamous cancer cell lines. Polymerase chain reaction (PCR) amplification revealed that five of the nine cell lines (55%) manifested homozygous deletions of CDKN2B, CDKN2, and/or flanking loci on chromosomal band 9p21. Reverse transcriptase-PCR (RT-PCR) was used to examine CDKN2 and CDKN2B mRNA in the nine cell lines. Lack of CDKN2 and CDKN2B mRNA correlated perfectly with homozygous deletion involving these genes. No subtle intragenic mutations of CDKN2B or CDKN2 were detected by DNA sequencing of their entire coding sequences in any cell lines lacking homozygous deletion. Two of the cell lines manifested homozygous deletions excluding CDKN2; one of these two deletions also excluded CDKN2B. These results suggest that inactivation of CDKN2B and CDKN2 may contribute to the malignant phenotype in esophageal cells and that homozygous deletion may be the predominant mechanism for inactivation of CDKN2B and CDKN2. Alternatively, a gene or genes adjacent to CDKN2B/CDKN2 may constitute the target(s) of deletion at this locus.
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PMID:Genomic DNA and messenger RNA expression alterations of the CDKN2B and CDKN2 genes in esophageal squamous carcinoma cell lines. 754 37

Ovarian-carcinoma cell lines (OVCAR3, IGROVI, OVCA432, SW626 and SKOV3), grown in standard medium containing supra-physiological (2.3 microM) folate concentration, display different levels of reactivity with the anti-folate-binding-protein (FBP) monoclonal antibody MOv18, which recognizes the alpha-isoform of the protein. Gel-filtration and absorption experiments indicated that on IGROVI cells this molecule accounts for all folic-acid binding at nanomolar concentrations. The aim of the study was to investigate the effect of extracellular folate levels on cells adapted to grow in medium containing physiological folate concentration (20 nM). By the ternary complex assay, all cell lines showed a marked depletion of intracellular reduced folates, compared with those in standard folate medium. The monitoring of FBP by MOv18 showed on IGROVI cells a transient up-regulation of the protein, whereas on the other cell lines, except SKOV3, no changes were detected. These data suggest that in these cells further over-expression of the molecule cannot generally be induced by lowering the extracellular folate concentration. On SKOV3, Scatchard analysis of 125I-MOv18 binding, as well as the evaluation of total folate binding capacity, showed a 2- to 3-fold stable increase of FBP expression after long-term growth in low-folate medium. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis indicated in these cells a 1.5-fold increase in alpha-FBP mRNA. SKOV3 cells, maintained in vitro in medium containing supraphysiological and physiological (i.e., low-folate) concentrations were injected into nude mice. Weight differences, though not statistically significant, were observed in favour of low-folate-derived tumors. Immunohistochemical and immunochemical analysis of the tumor samples showed that in SKOV3 cells the receptor modulation can also be induced by restoring the physiological folate concentration in vivo.
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PMID:Growth of ovarian-carcinoma cell lines at physiological folate concentration: effect on folate-binding protein expression in vitro and in vivo. 759 Dec 38


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