Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
about
Epidemiologic background of hand hygiene and evaluation of the most important agents for scrubs and rubsRelationship between triclosan and susceptibilities of bacteria isolated from hands in the communityThe isoniazid-NAD adduct is a slow, tight-binding inhibitor of InhA, the Mycobacterium tuberculosis enoyl reductase: adduct affinity and drug resistanceExposure of sink drain microcosms to triclosan: population dynamics and antimicrobial susceptibilityMolecular basis for triclosan activity involves a flipping loop in the active siteDesign and Synthesis of Aryl Ether Inhibitors of theBacillus AnthracisEnoyl-ACP ReductaseSlow-Onset Inhibition of the FabI Enoyl Reductase from Francisella tularensis : Residence Time and in Vivo ActivityDual-resolution molecular dynamics simulation of antimicrobials in biomembranesAntibacterial household products: cause for concernOn the need and speed of regulating triclosan and triclocarban in the United StatesImpairment of the bacterial biofilm stability by triclosanSignature gene expression profiles discriminate between isoniazid-, thiolactomycin-, and triclosan-treated Mycobacterium tuberculosisCharacterization of Pseudomonas aeruginosa enoyl-acyl carrier protein reductase (FabI): a target for the antimicrobial triclosan and its role in acylated homoserine lactone synthesisPredictive Studies Suggest that the Risk for the Selection of Antibiotic Resistance by Biocides Is Likely Low in Stenotrophomonas maltophiliaCross-resistance between triclosan and antibiotics in Pseudomonas aeruginosa is mediated by multidrug efflux pumps: exposure of a susceptible mutant strain to triclosan selects nfxB mutants overexpressing MexCD-OprJ.Mutational analysis of the triclosan-binding region of enoyl-ACP (acyl-carrier protein) reductase from Plasmodium falciparum.Potential impact of increased use of biocides in consumer products on prevalence of antibiotic resistanceThe impact of triclosan on the spread of antibiotic resistance in the environment.Sublethal triclosan exposure decreases susceptibility to gentamicin and other aminoglycosides in Listeria monocytogenesMutations upstream of fabI in triclosan resistant Staphylococcus aureus strains are associated with elevated fabI gene expression.Fatty acid biosynthesis as a target for novel antibacterialsIdentification and characterization of TriABC-OpmH, a triclosan efflux pump of Pseudomonas aeruginosa requiring two membrane fusion proteinsThe Francisella tularensis FabI enoyl-acyl carrier protein reductase gene is essential to bacterial viability and is expressed during infection.Plasmid selection in Escherichia coli using an endogenous essential gene marker.Reduced triclosan susceptibility in methicillin-resistant Staphylococcus epidermidis.Triclosan Resistome from Metagenome Reveals Diverse Enoyl Acyl Carrier Protein Reductases and Selective Enrichment of Triclosan Resistance Genes.Diversity in enoyl-acyl carrier protein reductases.Chronic arsenic exposure and microbial drug resistance.Targeting InhA, the FASII enoyl-ACP reductase: SAR studies on novel inhibitor scaffolds.Current and Emerging Topical Antibacterials and Antiseptics: Agents, Action, and Resistance Patterns.Transformation of triclosan by Trametes versicolor and Pycnoporus cinnabarinus.Antimicrobial biocides in the healthcare environment: efficacy, usage, policies, and perceived problems.Impact of exposure of methicillin-resistant Staphylococcus aureus to polyhexanide in vitro and in vivo.Characterization of triclosan-resistant mutants reveals multiple antimicrobial resistance mechanisms in Rhodospirillum rubrum S1H.Characterization of Mycobacterium smegmatis expressing the Mycobacterium tuberculosis fatty acid synthase I (fas1) gene.Disruption of key NADH-binding pocket residues of the Mycobacterium tuberculosis InhA affects DD-CoA binding ability.Altered NADH/NAD+ ratio mediates coresistance to isoniazid and ethionamide in mycobacteria.Triclosan inhibition of mycobacterial InhA in Saccharomyces cerevisiae: yeast mitochondria as a novel platform for in vivo antimycolate assays.Triclosan-induced genes Rv1686c-Rv1687c and Rv3161c are not involved in triclosan resistance in Mycobacterium tuberculosis.Distribution of triclosan-resistant genes in major pathogenic microorganisms revealed by metagenome and genome-wide analysis.
P2860
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P2860
Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
@en
Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
@nl
type
label
Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
@en
Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
@nl
prefLabel
Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
@en
Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan.
@nl
P2093
P2860
P356
P1476
Genetic evidence that InhA of Mycobacterium smegmatis is a target for triclosan
@en
P2093
L M McMurry
P F McDermott
P2860
P304
P356
10.1128/AAC.43.3.711
P407
P577
1999-03-01T00:00:00Z