Two novel point mutations in clinical Staphylococcus aureus reduce linezolid susceptibility and switch on the stringent response to promote persistent infection.
about
Persisters-as elusive as everResistance to linezolid caused by modifications at its binding site on the ribosomeStructural Basis for Methyl Transfer by a Radical SAM EnzymeWithin-host evolution of bacterial pathogens.Evolution of multidrug resistance during Staphylococcus aureus infection involves mutation of the essential two component regulator WalKRThe mechanism of heterogeneous beta-lactam resistance in MRSA: key role of the stringent stress responseAntibiotic activity against small-colony variants of Staphylococcus aureus: review of in vitro, animal and clinical data.The dominant Australian community-acquired methicillin-resistant Staphylococcus aureus clone ST93-IV [2B] is highly virulent and genetically distinctLow prevalence of Cfr-mediated linezolid resistance among methicillin-resistant Staphylococcus aureus in a Spanish hospital: case report on linezolid resistance acquired during linezolid therapy.Staphylococcus aureus Small Colony Variants (SCVs): a road map for the metabolic pathways involved in persistent infectionsEvolutionary and sequence-based relationships in bacterial AdoMet-dependent non-coding RNA methyltransferasesAdaptive evolution of Staphylococcus aureus during chronic endobronchial infection of a cystic fibrosis patient.Inactivation of thyA in Staphylococcus aureus attenuates virulence and has a strong impact on metabolism and virulence gene expression.Whole genome analysis of linezolid resistance in Streptococcus pneumoniae reveals resistance and compensatory mutations.Clinical significance of microbial infection and adaptation in cystic fibrosis.Secretome analysis defines the major role of SecDF in Staphylococcus aureus virulenceHigh-resolution transcriptomic analysis of the adaptive response of Staphylococcus aureus during acute and chronic phases of osteomyelitis.A regulatory feedback loop between RpoS and SpoT supports the survival of Legionella pneumophila in water.Prolonged growth of a clinical Staphylococcus aureus strain selects for a stable small-colony-variant cell type.Quorum sensing inhibitors increase the susceptibility of bacterial biofilms to antibiotics in vitro and in vivo.Inactivation of the indigenous methyltransferase RlmN in Staphylococcus aureus increases linezolid resistanceA naturally occurring single amino acid replacement in multiple gene regulator of group A Streptococcus significantly increases virulenceAnimals devoid of pulmonary system as infection models in the study of lung bacterial pathogensThe bacterial alarmone (p)ppGpp activates the type III secretion system in Erwinia amylovora.Colonization, pathogenicity, host susceptibility, and therapeutics for Staphylococcus aureus: what is the clinical relevance?ppGpp negatively impacts ribosome assembly affecting growth and antimicrobial tolerance in Gram-positive bacteriaImpact of daptomycin resistance on Staphylococcus aureus virulence.Determinants of tRNA Recognition by the Radical SAM Enzyme RlmN.Identification and Optimization of Carbon Radicals on Hydrated Graphene Oxide for Ubiquitous Antibacterial Coatings.The Escherichia coli RlmN methyltransferase is a dual-specificity enzyme that modifies both rRNA and tRNA and controls translational accuracy.Bacillithiol has a role in Fe-S cluster biogenesis in Staphylococcus aureus.Toward an understanding of the evolution of Staphylococcus aureus strain USA300 during colonization in community householdsThe insect Galleria mellonella as a powerful infection model to investigate bacterial pathogenesisClinical Significance and Pathogenesis of Staphylococcal Small Colony Variants in Persistent Infections.Antimicrobial resistance and virulence: a successful or deleterious association in the bacterial world?The RpoB H₄₈₁Y rifampicin resistance mutation and an active stringent response reduce virulence and increase resistance to innate immune responses in Staphylococcus aureus.Whole-genome sequencing reveals a link between β-lactam resistance and synthetases of the alarmone (p)ppGpp in Staphylococcus aureusDecreased vancomycin susceptibility in Staphylococcus aureus caused by IS256 tempering of WalKR expression.Improved understanding of factors driving methicillin-resistant Staphylococcus aureus epidemic wavesVirulence of vancomycin-resistant Enterococcus faecium according to linezolid resistance and clinical outbreak status.
P2860
Q26748708-96D20A67-F40F-434E-AABD-5EB6E7B8C419Q27006772-1EC0E6EE-5845-4D01-A5F1-E0D3886632DBQ27667611-930513B5-6EC4-4FE4-B7B6-6C095C170822Q28072013-CE7C3493-9DC8-4AB2-8BBA-54A09826841BQ28477900-9A3A012A-5299-4A3B-A34F-5C9EF4DAFD5FQ28536588-1302F655-511C-44C2-B989-5595DCCE35BEQ30597709-6014E44B-3468-448B-B59A-25E440E05CFFQ31032795-1A11F9DA-50B3-4A05-B915-00C5E9846767Q31114532-A61FDFDF-39F9-44C7-840A-D87AB89E8D0BQ33958329-40BF7EB6-A725-4779-A552-9514817231CFQ33989831-9549CA12-5115-4248-B793-5153622266B6Q34017905-4F5A3CA4-8174-46E5-9182-63008B4BE5E2Q34026284-BD8BA8A5-A2B4-47EE-B678-C76F780785C7Q34049640-768E9B7B-CED3-4F6F-B7B4-DF331FB2BF13Q34491552-53A783F6-98ED-4551-978A-A12701806415Q34713271-D7B5CAAB-A541-4981-A8CA-4409560684A6Q34782144-790BA943-E132-4AA1-9D0B-6A4F9FE82229Q34933421-CDBD40A7-17AD-42E1-881D-74E502D1C8D2Q34955578-95491F3F-E22E-485D-BC91-6881D03ECF5EQ35004955-43EC1394-366C-4A84-8CE1-5AC3C2A97991Q35005203-C97B9B2A-4E31-494C-8BF5-B5BA3B596C7CQ35008484-BC4572A9-D0FA-44E5-80D8-7125152E1169Q35048029-D0B8AC8F-580E-48A8-AD6F-9B7B250DA7E6Q35214799-3C1ED4C8-14E7-4E74-8076-5B531F8C0623Q35736907-7A485EC6-EF25-4DCD-8E72-70CFFAD50F40Q35948392-F297530B-07FF-4A72-AB51-7025D2EDA550Q36147127-16AEBC93-D7B5-43D9-B335-154A6F2206C1Q36208300-52B75059-2A9F-44E1-80CE-B7136B3AAA8BQ36233419-149659D0-C83D-4966-BCBE-B1DC217CFCF9Q36246613-E92F7C72-D402-43EF-8E8F-7E96724702E4Q36441404-DB92EA4B-2565-4203-A599-6539D771DCDFQ36525045-F7840091-405B-4F0E-863B-9E9C8EB4F25DQ36594846-C0885461-9C8F-4E24-9C26-338880DD1FB2Q36675223-3C0A5594-88CD-4473-86AC-2408EA4BD972Q36757725-107BE253-6636-46FD-B0F2-BCB43B2ADEF2Q36787486-7E2CD8F9-E88B-4BE9-B6BD-9977773E507AQ36870340-3BD9F48B-AEB1-4386-8A64-6BCCA6377015Q36969754-21C0FA7D-2703-4DDD-B277-821CE5794CABQ36999966-350CB257-90B7-4C7D-9434-31CB205A9915Q37036641-9F4C1A18-E19A-4DA6-87FC-BE63C52939B4
P2860
Two novel point mutations in clinical Staphylococcus aureus reduce linezolid susceptibility and switch on the stringent response to promote persistent infection.
description
2010 nî lūn-bûn
@nan
2010 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Two novel point mutations in c ...... promote persistent infection.
@ast
Two novel point mutations in c ...... promote persistent infection.
@en
type
label
Two novel point mutations in c ...... promote persistent infection.
@ast
Two novel point mutations in c ...... promote persistent infection.
@en
prefLabel
Two novel point mutations in c ...... promote persistent infection.
@ast
Two novel point mutations in c ...... promote persistent infection.
@en
P2093
P2860
P50
P1433
P1476
Two novel point mutations in c ...... promote persistent infection.
@en
P2093
Hyun-Woo Rhee
John K Davies
Jong-In Hong
Natasha E Holmes
Paul F Harrison
P2860
P304
P356
10.1371/JOURNAL.PPAT.1000944
P577
2010-06-10T00:00:00Z