Development of a competitive index assay to evaluate the virulence of Listeria monocytogenes actA mutants during primary and secondary infection of mice.
about
Listeria monocytogenes traffics from maternal organs to the placenta and backH2-M3-restricted CD8+ T cells are not required for MHC class Ib-restricted immunity against Listeria monocytogenesDevelopment of multiple strain competitive index assays for Listeria monocytogenes using pIMC; a new site-specific integrative vectorShort-term genome evolution of Listeria monocytogenes in a non-controlled environmentConstitutive activation of PrfA tilts the balance of Listeria monocytogenes fitness towards life within the host versus environmental survivalSigma B contributes to PrfA-mediated virulence in Listeria monocytogenes.Listeria monocytogenes PrsA2 is required for virulence factor secretion and bacterial viability within the host cell cytosol.Branched-chain fatty acids promote Listeria monocytogenes intracellular infection and virulence.An adhesion protein of Salmonella enterica serovar Typhi is required for pathogenesis and potential target for vaccine development.Actin polymerization drives septation of Listeria monocytogenes namA hydrolase mutants, demonstrating host correction of a bacterial defect.The cell biology of Listeria monocytogenes infection: the intersection of bacterial pathogenesis and cell-mediated immunity.The Listeria monocytogenes hibernation-promoting factor is required for the formation of 100S ribosomes, optimal fitness, and pathogenesis.The Listeria monocytogenes lemA gene product is not required for intracellular infection or to activate fMIGWII-specific T cellsListeria monocytogenes mutants that fail to compartmentalize listerolysin O activity are cytotoxic, avirulent, and unable to evade host extracellular defenses.Analysis of the σE regulon in Crohn's disease-associated Escherichia coli revealed involvement of the waaWVL operon in biofilm formation.Listeria monocytogenes flagella are used for motility, not as adhesins, to increase host cell invasion.Compartmentalization of the broad-range phospholipase C activity to the spreading vacuole is critical for Listeria monocytogenes virulence.Listeriosis in the pregnant guinea pig: a model of vertical transmission.Comprehensive identification of virulence factors required for respiratory melioidosis using Tn-seq mutagenesisListeriolysin O secreted by Listeria monocytogenes into the host cell cytosol is degraded by the N-end rule pathway.Identification of novel Listeria monocytogenes secreted virulence factors following mutational activation of the central virulence regulator, PrfA.SecA2-dependent secretion of autolytic enzymes promotes Listeria monocytogenes pathogenesis.Mice lacking the type I interferon receptor are resistant to Listeria monocytogenesLplA1-dependent utilization of host lipoyl peptides enables Listeria cytosolic growth and virulence.The Listeria monocytogenes ChiA chitinase enhances virulence through suppression of host innate immunity.A Listeria monocytogenes mutant defective in bacteriophage attachment is attenuated in orally inoculated mice and impaired in enterocyte intracellular growth.Stable integration vector for nutrient broth-based selection of attenuated Listeria monocytogenes strains with recombinant antigen expressionGeneration of branched-chain fatty acids through lipoate-dependent metabolism facilitates intracellular growth of Listeria monocytogenes.Development of a mariner-based transposon and identification of Listeria monocytogenes determinants, including the peptidyl-prolyl isomerase PrsA2, that contribute to its hemolytic phenotype.The meningococcal ABC-Type L-glutamate transporter GltT is necessary for the development of experimental meningitis in miceInlP, a New Virulence Factor with Strong Placental Tropism.Activity of the Pore-Forming Virulence Factor Listeriolysin O Is Reversibly Inhibited by Naturally Occurring S-Glutathionylation.The σE pathway is involved in biofilm formation by Crohn's disease-associated adherent-invasive Escherichia coli.Listeria monocytogenes adapts to long-term stationary phase survival without compromising bacterial virulence.Structure to function of an α-glucan metabolic pathway that promotes Listeria monocytogenes pathogenesis.Immunology: Stillbirth prevented by signal blockade.Apparent role for Borrelia burgdorferi LuxS during mammalian infection.Exploration of the role of the non-coding RNA SbrE in L. monocytogenes stress response.Intragastric inoculation with a cocktail of Listeria monocytogenes strains does not potentiate the severity of infection in A/J mice compared to inoculation with the individual strains comprising the cocktail.Controlled branched-chain amino acids auxotrophy in Listeria monocytogenes allows isoleucine to serve as a host signal and virulence effector.
P2860
Q27320190-9A17DB7F-37CE-4D2D-B855-70BF591E01F0Q28505940-F5863DC7-DFD8-4198-8B72-528A04840233Q30844415-5E4BF20B-AF20-4FA4-9A71-F36A3660B484Q33384897-C47AC04F-332C-4B0F-A52A-BE2952610CF5Q33769460-CF8017D7-E715-468F-A034-1CA49B843FB5Q34125482-28131EA9-0F53-46FF-958E-6BA681045417Q34290715-89A290A2-2AEA-42FE-B135-EE0999F3772BQ34290837-BEA0E80B-6ED3-478F-A396-BCEF72E59DEEQ34602404-1D564BE9-838C-4730-87F6-BDB689023C2BQ34740282-40531A9A-D014-4705-80CA-B8DF900358EFQ34774585-3A1C7395-2B15-4527-B3D0-641695029475Q34853421-E08B1A53-064D-4745-8569-9C4C80FBADE4Q34944103-6397F6C8-D629-4CFD-9229-334E62097D90Q34947257-7848069A-91FF-43D3-9FDE-D4338DCD6E61Q35214807-78C3A31C-8124-4D45-BD48-8A9FF0B85A2BQ35220345-AB3E0A4D-6754-4E23-A544-8246DE73BA8CQ35689107-0878B8E8-68AE-442D-B63D-0E8B56420172Q36227927-6B28637F-3CDD-445B-A565-3C8C9C4AA2C1Q36245628-6B54D283-174C-4FDF-9963-E51BBE876B5FQ36313828-AF422D4D-42A6-45CA-B519-5ECC3EC0AF3EQ36313978-941F336B-115E-4CCC-B92A-DBC7E0EF6388Q36350571-6A60A4CE-DB5D-4ADA-A189-1F1E4BB70A9BQ36399578-BA6724E2-CC3D-45B2-B8D1-B8BC6F054C6DQ36631559-AF3FD224-9D89-40B2-8537-E65D7A51BE2DQ36706238-33F05E80-078B-430A-A385-BCAC7F062D76Q36845273-914E36BF-A141-4F99-9706-BD329676E3BEQ36897998-DC796A51-5D4A-4F97-8CBD-FF455F93C106Q37127810-64B2DF61-13FC-4C73-B0F2-A2883D5A2A17Q37232523-C05B72A2-C740-4252-A37F-9B0145E086A5Q37333380-5F051047-630E-43D1-BEF3-79EF3392EF9DQ37425026-4B977C80-46B1-430D-A1C9-1332272DFE92Q38718753-8DC4141B-49C9-4EEE-80E8-3E5470F62E89Q39252460-A5BD5686-CD68-4F74-9F81-BF279144B055Q39472443-2E5209E2-D56C-49D0-9944-15F7F5123344Q40461505-FB625BC6-29B4-48B1-9B93-E9B2B8F15913Q41272781-3617C5E6-FFE8-4988-A917-60437ECD3804Q41531292-5C218F5B-0AF6-423B-B48D-A676D6D43C20Q43181671-1DB4A52F-E319-400C-9168-E73297AEA172Q44672545-AC04725F-44B3-4615-8C03-D381B6682523Q54257865-B05C82E0-180C-4E9F-AE40-A30B41B70F9A
P2860
Development of a competitive index assay to evaluate the virulence of Listeria monocytogenes actA mutants during primary and secondary infection of mice.
description
2001 nî lūn-bûn
@nan
2001 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Development of a competitive i ...... d secondary infection of mice.
@ast
Development of a competitive i ...... d secondary infection of mice.
@en
Development of a competitive i ...... d secondary infection of mice.
@nl
type
label
Development of a competitive i ...... d secondary infection of mice.
@ast
Development of a competitive i ...... d secondary infection of mice.
@en
Development of a competitive i ...... d secondary infection of mice.
@nl
prefLabel
Development of a competitive i ...... d secondary infection of mice.
@ast
Development of a competitive i ...... d secondary infection of mice.
@en
Development of a competitive i ...... d secondary infection of mice.
@nl
P2093
P2860
P1476
Development of a competitive i ...... d secondary infection of mice.
@en
P2093
P2860
P304
P356
10.1128/IAI.69.9.5953-5957.2001
P407
P577
2001-09-01T00:00:00Z