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)

To investigate gene organization and expression signals in extreme thermophilic archaebacteria, tRNA genes were cloned from Thermoproteus tenax. Clones for five tRNA species were obtained, namely for tRNAAla (TGC), tRNAAla (CGC), tRNALeu (CAG), tRNALeu (CAA) and tRNAMet (CAT). Three of the respective genes were located singly in the chromosome, the two others (tRNAAla and tRNAMet) were clustered but in a head to head position. Four of the genes contained intervening sequences, either in the classical position 3' to the anticodon (tRNAMet), or within the anticodon sequence (tRNALeuCAG), or in the hitherto unique position 5' to the anticodon within the anticodon stem region (tRNAAla). Existence of a transcript containing the intervening sequence was demonstrated by nuclease S1 mapping. All tRNA genes were extremely rich in G-C basepairs of helical regions, a feature which may contribute to thermostability of the secondary structure. The start site of transcription of the 16S/23S rRNA operon and of two tRNA genes of Thermoproteus was determined by nuclease S1 mapping. Transcription of the tRNA genes initiates close to or immediately at the 5' end of the structural gene, that of the rRNA operon 175 bp upstream of the coding region. About 18 bp upstream of the transcription initiation site a conserved AT-rich sequence motif occurs within a fairly GC-rich intercistronic spacer. Its putative instability at the high growth temperature of Thermoproteus suggests a function as entry site for RNA polymerase.
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PMID:Genes for stable RNA in the extreme thermophile Thermoproteus tenax: introns and transcription signals. 1598 38

Nucleotide changes in catalase peroxidase (Kat G) gene and gene encoding the beta subunit of RNA polymerase (rpo B), responsible for isoniazid and rifampicin drug resistance were determined in the clinical isolates of Mycobacterium tuberculosis by PCR-RFLP, Line probe assay and DNA sequencing. PCR-RFLP test was performed by HapII cleavage of an amplified fragment of Kat G gene to detect the transversion 315AGC-->ACC(Ser-->Thr) which is associated with INH drug resistance. The Line probe assay kit was evaluated to detect the mutation in 81bp RMP resistance determining region of rpo B gene associated with RMP drug resistance. These results were validated by DNA sequencing and drug susceptibility test. Kat G S 315 T mutation was found in 74.19% strains of M. tuberculosis from Delhi. This mutation was not found in any of the susceptible strains tested. The line probe assay kit and DNA sequencing identified 18 isolates as RMP resistant with specific mutation, while one of the RMP resistant strain was identified as RMP susceptible, with a concordance of 94.73% with the phenotypic drug susceptibility result. Majority (8 of 19, 42.1%) of resistant isolates involved base changes at codon 531 of rpo B gene. Both PCR-RFLP and Line probe assay test can be used in many of the clinical microbiology laboratories for early detection of isoniazid and rifampicin drug resistance in clinical isolates of M. tuberculosis.
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PMID:Molecular characterization of mutation associated with rifampicin and isoniazid resistance in Mycobacterium tuberculosis isolates. 1687 43

Human tuberculosis is still one of the most frequent causes of death worldwide. Despite the implementation of therapeutic regimes combining four drugs, the rise of resistant and multidrug-resistant Mycobacterium tuberculosis strains has compromised their efficacy. Two of the most effective anti-tubercular drugs in use, rifampicin and isoniazid, have been closely studied due to their therapeutic importance. These studies have led to the identification of the genes involved in resistance mechanisms and of those encoding the molecular targets for these drugs. Rifampicin is an inhibitor of the beta-subunit of the RNA polymerase of prokaryotes, including M. tuberculosis. Resistance to rifampicin is mediated by mutations clustered in a small region of the rpoB gene. A fraction of resistant strains showed no mutations in rpoB, suggesting that other mechanisms of resistance, possibly efflux pumps, may exist. Isoniazid is a pro-drug activated by KatG, a catalase-peroxidase. Mutations in katG, the most commonly found in M. tuberculosis clinical isolates, give high levels of resistance. In spite of this, the molecular target for isoniazid is InhA, an enoyl-ACP-reductase involved in the biosynthesis of mycolic acids. Other mutations causing resistance to isoniazid have been mapped to ndh, a gene encoding the NADH dehydrogenase.
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PMID:[Mechanisms of action of and resistance to rifampicin and isoniazid in Mycobacterium tuberculosis: new information on old friends]. 1703 59

Alpha amanitin is a powerful natural hepatotoxin that belongs to the amatoxins isolated from deadly poisonous Amanita phalloides mushroom. The basic molecular mechanism of their toxicity was attributed to inhibition of RNA polymerase II of the eukaryotic cells. At present, the most effective clinical antidote to acute Amanita phalloides mushroom poisoning is silybin, an antioxidant possessing free radical scavenger activity and inhibiting lipid peroxidation, stabilizing membrane structure and protecting enzymes under conditions of oxidative stress. Bearing in mind the biological mechanism of silybin action and the fact that for different amatoxins (alpha, beta, and est. amanitins) does not established straight correlation between their in vivo LD50 and inhibitory constants (Ki) toward RNA polymerase III in vitro determined we supposed some additional toxic effects of these toxins might contribute to their severe hepatotoxicity. Our formerly in vitro experiments demonstrated that alpha amanitin could act either as an antioxidant or as a prooxidant depending on the treatment conditions and toxin concentration. By UV-visible spectroscopy we also shown that alpha amanitin was sensitive to oxidation by a system of lactoperoxidase/H(2)O(2) and assumed formation of free radical toxin intermediates. Having in mind some exogenic compounds including natural toxins can induce increased production of reactive oxygen species (ROS) we suggested similar generation of ROS provoked by alpha amanitin. Our recently in vitro studies have demonstrated that the alpha amanitin could increase superoxide dismutase (SOD) activity and inhibit catalase (CAT) activity to a considerable degree after together incubation of the toxin with any of enzymes. We have also shown that in vitro increased SOD activity was due to superoxide anion radical scavenging activity (SSA) of the toxin. This therefore informed the decision to study the in vivo effect of alpha amanitin on SOD and CAT activity and the level of lipid peroxidation (LPO) products in liver homogenates isolated from mice treated with the toxin. Statistical significant increased level of LPO products was found at the 6th day comparing to the 20th hour after mice treatment with a subletal dose of the toxin. Based on our previous in vitro and present in vivo studies we have made a hypothesize that in vivo during liver accumulation of the toxin it might be transformed to free radical intermediates causing increase in ROS levels. As a result a peroxidative process in hepatocytes might contribute to the severe alpha amanitin hepatotoxicity.
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PMID:Free radical reactions might contribute to severe alpha amanitin hepatotoxicity--a hypothesis. 1733 61

Five coagulase-negative, novobiocin-susceptible staphylococcal strains were isolated from human blood cultures in different German and Belgian medical facilities. A novel species, 'Staphylococcus pettenkoferi' was proposed recently to accommodate two of these strains (B3117(T) and A6664), although the name was not validly published. All five strains belonged to the genus Staphylococcus because they were non-motile, Gram-positive, catalase-positive cocci with peptidoglycan type (A3 alpha type L-lys-gly(2-4)-L-Ser-Gly), menaquinone pattern (MK-7, MK-6 and MK-8) and major cellular fatty acids (ai-C(15 : 0), ai-C(17 : 0) and i-C(15 : 0)) that corresponded to those of staphylococci. Phenotypically, the isolates most closely resembled Staphylococcus capitis subsp. capitis and Staphylococcus auricularis, but they could be distinguished from these species by physiological tests and chemotaxonomic investigations. The results of DNA-DNA hybridization, chemotaxonomic investigations and 16S rRNA gene and RNA polymerase B gene (rpoB) sequence analysis enabled strains B3117(T), K6999, 229 and 230 to be differentiated genotypically and phenotypically from known Staphylococcus species, indicating that these isolates are representatives of a novel species. The name Staphylococcus pettenkoferi sp. nov. is proposed for this novel species, with strain B3117(T) (=CIP 107711(T)=CCUG 51270(T)) as the type strain. Due to differences in the results of physiological and chemotaxonomic investigations and DNA-DNA hybridization data, strain A6664 was not included in the description of the novel species.
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PMID:Staphylococcus pettenkoferi sp. nov., a novel coagulase-negative staphylococcal species isolated from human clinical specimens. 1762 91

Dietary fat accelerates the ageing process and causes a greater mortality by accumulating lipid hydroperoxide (LPO) in Drosophila melanogaster. The present study found that the life span of D. melanogaster was shortened from 54 to 6 days in a dose-dependent manner when fat in diet increased from 0% to 25%. The results showed that supplementation of both green tea catechins (GTC) and broccoli extract (BE) reversed partially the fat-induced mortality. The maximum life span was 44 days for the control group fed with a 5% fat, whereas it increased to 50 and 59 days in the GTC- and BE-supplemented groups, respectively. The 50% survival time for the control flies fed with a 5% fat diet was 30 days. In contrast, it increased to 32 and 48 days when GTC and BE were supplemented in the diet. This was consistent with a significant reduction in total body LPO level in D. melanogaster maintained on the GTC- and BE-supplemented diet. Accordingly, catalase and superoxide dismutase (SOD) activities increased significantly in the flies fed with a GTC or a BE diet compared with those fed with a control 5% fat diet. Reverse transcriptase-polymerase chain reaction analysis indicated that the increase in enzymatic activities of catalase and SOD was accompanied by up-regulation of genes for catalase, copper-zinc containing SOD and manganese-containing SOD. It was concluded that GTC and BE reversed the fat-induced mortality in D. melanogaster, most likely but necessarily solely, by up-regulation of endogenous antioxidant enzymes.
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PMID:Green tea catechins and broccoli reduce fat-induced mortality in Drosophila melanogaster. 1770 29

A Gram-positive and catalase-negative coccus that formed chains, strain FP15-1(T), isolated from fermented tea leaves ('miang'), was studied systematically. The strain was facultatively anaerobic and produced l-lactic acid from glucose. Demethylmenaquinone (DMK-7) was the major menaquinone. Straight-chain unsaturated fatty acids C(16 : 1) and C(18 : 1) were the dominant components. The DNA G+C content was 37.8 mol%. On the basis of 16S rRNA and RNA polymerase alpha subunit (rpoA) gene sequence analysis, strain FP15-1(T) was closely related to Enterococcus italicus KCTC 5373(T), with 99.2 and 93.8 % similarity, respectively. The strain could be clearly distinguished from E. italicus ATCC 5373(T) by low DNA-DNA relatedness (< or =33.8 %) and phenotypic characteristics. Therefore, this strain represent a novel species of the genus Enterococcus, for which the name Enterococcus camelliae sp. nov. is proposed. The type strain is FP15-1(T) (=KCTC 13133(T) =NBRC 101868(T) =NRIC 0105(T) =TISTR 932(T) =PCU 277(T)).
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PMID:Enterococcus camelliae sp. nov., isolated from fermented tea leaves in Thailand. 1776 90

A Gram-positive and catalase-negative coccus that formed chains, designated strain FP48-3(T), isolated from fermented sausage ('mum'), was studied systematically. Strain FP48-3(T) was facultatively anaerobic and produced l-lactic acid from glucose. Straight-chain fatty acids C(18 : 1) and C(16 : 0) were the dominant components. The DNA G+C content of strain FP48-3(T) was 37.9 mol%. On the basis of 16S rRNA and RNA polymerase alpha-subunit (rpoA) gene sequence analysis, strain FP48-3(T) was closely related to Enterococcus hirae LMG 6399(T), Enterococcus durans LMG 10746(T) and Enterococcus faecium LMG 11423(T), with 99.3-99.6 and 95.1-96.9 % sequence similarities, respectively. Strain FP48-3(T) could be clearly distinguished from E. hirae LMG 6399(T), E. durans LMG 10746(T) and E. faecium LMG 11423(T) by low DNA-DNA relatedness (< or =14 %) and phenotypic characteristics. Therefore, this strain represents a novel species of the genus Enterococcus, for which the name Enterococcus thailandicus sp. nov. is proposed. The type strain is FP48-3(T) (=KCTC 13134(T)=NBRC 101867(T)=NRIC 0107(T)=TISTR 933(T)=PCU 282(T)).
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PMID:Enterococcus thailandicus sp. nov., isolated from fermented sausage ('mum') in Thailand. 1859 7

Slowly growing, non-chromogenic mycobacteria were isolated from striped barombi mbo cichlids (Stomatepia mariae) maintained at the London Zoo Aquarium, UK. The isolates could be differentiated from other slowly growing, non-pigmented mycobacteria by a combination of phenotypic features including their inability to grow at 37 degrees C, positive tests for heat-stable catalase, tellurite reduction and arylsulfatase activity, and the absence of urease activity, Tween 80 hydrolysis, nitrate reductase, iron uptake and semiquantitative catalase. The almost full-length 16S rRNA gene sequence, together with partial sequences from the 65 kDa heat-shock protein (hsp65) and the beta-subunit of the bacterial RNA polymerase (rpoB) genes and the 16S-23S internal transcribed spacer 1 (ITS 1) region were identical for all three novel strains, but distinct from those of all known mycobacterial species. Phylogenetic analysis based on 16S rRNA gene sequences placed the novel isolates within the slowly growing mycobacteria group in close proximity to Mycobacterium florentinum. Based on genotypic and phenotypic findings, it is proposed that these isolates represent a novel species of the genus Mycobacterium, for which the name Mycobacterium stomatepiae sp. nov. is proposed with strain T11(T) (=DSM 45059(T)=CIP 109275(T)=NCIMB 14252(T)) as the type strain.
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PMID:Mycobacterium stomatepiae sp. nov., a slowly growing, non-chromogenic species isolated from fish. 1906 66

Activated pancreatic stellate cells (PSC) play a central role in the pathogenesis of pancreatic fibrosis, a common feature of chronic pancreatitis which is often caused by excessive alcohol consumption. In view of the central role of connective tissue growth factor (CCN2) in fibrosis, we investigated the mechanisms by which CCN2 is regulated in PSC following their exposure to ethanol or acetaldehyde. Primary cultures of PSC from Balb/c mice were treated with 0-50 mM ethanol or 0-200 microM acetaldehyde in the presence or absence of 4-methylpyrazole (4MP; an inhibitor of alcohol dehydrogenase), diallyl sulfide (DAS; an inhibitor of cytochrome P4502E1) or anti-oxidant catalase or vitamin D. CCN2 production, assessed by reverse-transcriptase polymerase chain reaction to measure CCN2 mRNA levels or by fluorescence activated cell sorting to assess CCN2 protein, was enhanced in a dose-dependent manner by ethanol or acetaldehyde. In the presence of 4MP, DAS, or the anti-oxidants vitamin D or catalase, there was a substantial decrease in the ability of ethanol to stimulate CCN2 mRNA expression and a concomitant decrease in CCN2-positive PSC. Accumulation of reactive oxygen species in PSC after exposure to ethanol was verified by loading the cells with dichlorofluorescin diacetate and showing that there was a stimulation of its oxidized fluorescent product, the latter of which was diminished in the presence of catalase or vitamin D. These results show the production of acetaldehyde and oxidant stress in mouse PSC are the cause of increased CCN2 mRNA and protein production after exposure of the cells to ethanol. The potential therapeutic effects of inhibitors of ethanol metabolism or anti-oxidants in alcoholic pancreatitis may arise in part through their ability to attenuate CCN2 production by PSC.
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PMID:Ethanol-mediated expression of connective tissue growth factor (CCN2) in mouse pancreatic stellate cells. 1928 Apr 52


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