Highly frequent mutations in negative regulators of multiple virulence genes in group A streptococcal toxic shock syndrome isolates. - Wikidata - awgldk - TriplyDB

Highly frequent mutations in negative regulators of multiple virulence genes in group A streptococcal toxic shock syndrome isolates.

Highly frequent mutations in negative regulators of multiple virulence genes in group A streptococcal toxic shock syndrome isolates.

http://www.wikidata.org/entity/Q33549662

about

The trans-kingdom identification of negative regulators of pathogen hypervirulence Molecular epidemiology and genomics of group A Streptococcus Thermoregulation of capsule production by Streptococcus pyogenes Evolutionary Constraints Shaping Streptococcus pyogenes-Host Interactions.Distinct single amino acid replacements in the control of virulence regulator protein differentially impact streptococcal pathogenesis Complete Genome Sequence of emm1 Streptococcus pyogenes A20, a Strain with an Intact Two-Component System, CovRS, Isolated from a Patient with Necrotizing Fasciitis.Dual-site phosphorylation of the control of virulence regulator impacts group a streptococcal global gene expression and pathogenesis Differences in SpeB protease activity among group A streptococci associated with superficial, invasive, and autoimmune disease.Streptococcal collagen-like protein A and general stress protein 24 are immunomodulating virulence factors of group A Streptococcus.Importance of whole genome sequencing for the assessment of outbreaks in diagnostic laboratories: analysis of a case series of invasive Streptococcus pyogenes infections.Signal transduction through CsrRS confers an invasive phenotype in group A Streptococcus.Group A Streptococcus secreted esterase hydrolyzes platelet-activating factor to impede neutrophil recruitment and facilitate innate immune evasion Streptolysin O and NAD-glycohydrolase prevent phagolysosome acidification and promote group A Streptococcus survival in macrophages.Intracellular Streptococcus pyogenes in human macrophages display an altered gene expression profile.The contribution of group A streptococcal virulence determinants to the pathogenesis of sepsis.Disease manifestations and pathogenic mechanisms of Group A Streptococcus.Group A streptococci clones associated with invasive infections and pharyngitis in Portugal present differences in emm types, superantigen gene content and antimicrobial resistance.Mutual exclusivity of hyaluronan and hyaluronidase in invasive group A Streptococcus.Partial loss of CovS function in Streptococcus pyogenes causes severe invasive disease The human antimicrobial peptide LL-37 binds directly to CsrS, a sensor histidine kinase of group A Streptococcus, to activate expression of virulence factors.Naturally occurring single amino acid replacements in a regulatory protein alter streptococcal gene expression and virulence in mice.Characterization of the effect of the histidine kinase CovS on response regulator phosphorylation in group A Streptococcus.Travel-related Streptococcal toxic shock syndrome caused by emm type 78 Streptococcus pyogenes.Mutations in the control of virulence sensor gene from Streptococcus pyogenes after infection in mice lead to clonal bacterial variants with altered gene regulatory activity and virulence.Parameters governing invasive disease propensity of non-M1 serotype group A streptococci.Serotype M3 and M28 Group A Streptococci Have Distinct Capacities to Evade Neutrophil and TNF-α Responses and to Invade Soft Tissues.Polymorphisms in regulator of protease B (RopB) alter disease phenotype and strain virulence of serotype M3 group A Streptococcus Interferon-γ-producing immature myeloid cells confer protection against severe invasive group A Streptococcus infections Population genomics: an investigative tool for epidemics.Contemporary Pharyngeal and Invasive emm1 and Invasive emm12 Group A Streptococcus Isolates Exhibit Similar In Vivo Selection for CovRS Mutants in Mice.The Mga Regulon but Not Deoxyribonuclease Sda1 of Invasive M1T1 Group A Streptococcus Contributes to In Vivo Selection of CovRS Mutations and Resistance to Innate Immune Killing Mechanisms.Immunization with a streptococcal multiple-epitope recombinant protein protects mice against invasive group A streptococcal infection Vitamin D and the human antimicrobial peptide LL-37 enhance group a streptococcus resistance to killing by human cells Regulatory rewiring confers serotype-specific hyper-virulence in the human pathogen group A Streptococcus Regulation of inhibition of neutrophil infiltration by the two-component regulatory system CovRS in subcutaneous murine infection with group A streptococcus Spontaneous mutations in Streptococcus pyogenes isolates from streptococcal toxic shock syndrome patients play roles in virulence.LacR mutations are frequently observed in Streptococcus intermedius and are responsible for increased intermedilysin production and virulence Complement-mediated opsonization of invasive group A Streptococcus pyogenes strain AP53 is regulated by the bacterial two-component cluster of virulence responder/sensor (CovRS) system.Presence of a Prophage Determines Temperature-Dependent Capsule Production in Streptococcus pyogenes.Repression of Rgg But Not Upregulation of LacD.1 in emm1-type covS Mutant Mediates the SpeB Repression in Group A Streptococcus.

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P2860

Highly frequent mutations in negative regulators of multiple virulence genes in group A streptococcal toxic shock syndrome isolates.

http://www.wikidata.org/entity/Q33549662

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2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2010 թվականի ապրիլին հրատարակված գիտական հոդված

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2010年の論文

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Haruo Watanabe

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Hideki Hasegawa

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Kazuo Kobayashi

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Manabu Ato

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Tadayoshi Ikebe

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Takayuki Matsumura

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P2860

Genome sequence of an M3 strain of Streptococcus pyogenes reveals a large-scale genomic rearrangement in invasive strains and new insights into phage evolution

Genome sequence of a serotype M3 strain of group A Streptococcus: phage-encoded toxins, the high-virulence phenotype, and clone emergence.

Genome-wide analysis of group a streptococci reveals a mutation that modulates global phenotype and disease specificity.

Identification of novel cytolytic peptides as key virulence determinants for community-associated MRSA

Identification of Rgg-regulated exoproteins of Streptococcus pyogenes.

Incompetence of neutrophils to invasive group A streptococcus is attributed to induction of plural virulence factors by dysfunction of a regulator.

A naturally occurring mutation in ropB suppresses SpeB expression and reduces M1T1 group A streptococcal systemic virulence.

Antimicrobial susceptibility survey of Streptococcus pyogenes isolated in Japan from patients with severe invasive group A streptococcal infections

A role for trigger factor and an rgg-like regulator in the transcription, secretion and processing of the cysteine proteinase of Streptococcus pyogenes.

The rgg gene of Streptococcus pyogenes NZ131 positively influences extracellular SPE B production.

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