Streptolysin O promotes group A Streptococcus immune evasion by accelerated macrophage apoptosis.
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Regulation of ATG4B stability by RNF5 limits basal levels of autophagy and influences susceptibility to bacterial infectionInflammasome/IL-1β Responses to Streptococcal PathogensCoiled-coil irregularities of the M1 protein structure promote M1-fibrinogen interaction and influence group A Streptococcus host cell interactions and virulence.Dnase1L3 Regulates Inflammasome-Dependent Cytokine Secretion.Evolutionary pathway to increased virulence and epidemic group A Streptococcus disease derived from 3,615 genome sequences.Genetic switch to hypervirulence reduces colonization phenotypes of the globally disseminated group A streptococcus M1T1 clone.Inhibition of Inflammasome-Dependent Interleukin 1β Production by Streptococcal NAD+-Glycohydrolase: Evidence for Extracellular Activity.The 4.5S RNA component of the signal recognition particle is required for group A Streptococcus virulenceSpecific behavior of intracellular Streptococcus pyogenes that has undergone autophagic degradation is associated with bacterial streptolysin O and host small G proteins Rab5 and Rab7M protein and hyaluronic acid capsule are essential for in vivo selection of covRS mutations characteristic of invasive serotype M1T1 group A Streptococcus.Group A Streptococcus secreted esterase hydrolyzes platelet-activating factor to impede neutrophil recruitment and facilitate innate immune evasionStreptolysin O and NAD-glycohydrolase prevent phagolysosome acidification and promote group A Streptococcus survival in macrophages.Responses of innate immune cells to group A Streptococcus.Role of pore-forming toxins in bacterial infectious diseases.The pore-forming toxin β hemolysin/cytolysin triggers p38 MAPK-dependent IL-10 production in macrophages and inhibits innate immunity.Disease manifestations and pathogenic mechanisms of Group A Streptococcus.Enterococcus faecalis infection activates phosphatidylinositol 3-kinase signaling to block apoptotic cell death in macrophages.The cholesterol-dependent cytolysins pneumolysin and streptolysin O require binding to red blood cell glycans for hemolytic activityIntegrating '-omics' and natural product discovery platforms to investigate metabolic exchange in microbiomesHost responses to group a streptococcus: cell death and inflammationA group A Streptococcus ADP-ribosyltransferase toxin stimulates a protective interleukin 1β-dependent macrophage immune responseSerine/threonine phosphatase (SP-STP), secreted from Streptococcus pyogenes, is a pro-apoptotic protein.Cationic antimicrobial peptide resistance mechanisms of streptococcal pathogens.Streptolysin S Promotes Programmed Cell Death and Enhances Inflammatory Signaling in Epithelial Keratinocytes during Group A Streptococcus Infection.Conquering Neutrophils.The Streptococcus pyogenes NAD(+) glycohydrolase modulates epithelial cell PARylation and HMGB1 releaseThe Influence of Programmed Cell Death in Myeloid Cells on Host Resilience to Infection with Legionella pneumophila or Streptococcus pyogenes.Genome Analysis of Streptococcus pyogenes Associated with Pharyngitis and Skin Infections.Streptolysin O Rapidly Impairs Neutrophil Oxidative Burst and Antibacterial Responses to Group A Streptococcus.Vitamin D and the human antimicrobial peptide LL-37 enhance group a streptococcus resistance to killing by human cellsRegulation of inhibition of neutrophil infiltration by the two-component regulatory system CovRS in subcutaneous murine infection with group A streptococcusDiffering Efficacies of Lead Group A Streptococcal Vaccine Candidates and Full-Length M Protein in Cutaneous and Invasive Disease ModelsIntergenic Variable-Number Tandem-Repeat Polymorphism Upstream of rocA Alters Toxin Production and Enhances Virulence in Streptococcus pyogenesIgG protease Mac/IdeS is not essential for phagocyte resistance or mouse virulence of M1T1 group A StreptococcusCharacterization of streptococcal platelet-activating factor acetylhydrolase variants that are involved in innate immune evasion.Activation of the Nlrp3 inflammasome by Streptococcus pyogenes requires streptolysin O and NF-kappa B activation but proceeds independently of TLR signaling and P2X7 receptor.Procaspase 8 and Bax are up-regulated by distinct pathways in Streptococcal pyrogenic exotoxin B-induced apoptosis.An extracellular bacterial pathogen modulates host metabolism to regulate its own sensing and proliferation.IL-1β is an innate immune sensor of microbial proteolysis.Neutrophils select hypervirulent CovRS mutants of M1T1 group A Streptococcus during subcutaneous infection of mice
P2860
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P2860
Streptolysin O promotes group A Streptococcus immune evasion by accelerated macrophage apoptosis.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
Streptolysin O promotes group ...... elerated macrophage apoptosis.
@en
Streptolysin O promotes group ...... elerated macrophage apoptosis.
@nl
type
label
Streptolysin O promotes group ...... elerated macrophage apoptosis.
@en
Streptolysin O promotes group ...... elerated macrophage apoptosis.
@nl
prefLabel
Streptolysin O promotes group ...... elerated macrophage apoptosis.
@en
Streptolysin O promotes group ...... elerated macrophage apoptosis.
@nl
P2093
P2860
P50
P356
P1476
Streptolysin O promotes group ...... elerated macrophage apoptosis.
@en
P2093
Anjuli M Timmer
Guy S Salvesen
John C Timmer
Mariam Ghochani
Terrence G Frey
P2860
P304
P356
10.1074/JBC.M804632200
P407
P577
2008-11-11T00:00:00Z