Molecular pathogenesis of neonatal group B streptococcal infection: no longer in its infancy.
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The surface protein Srr-1 of Streptococcus agalactiae binds human keratin 4 and promotes adherence to epithelial HEp-2 cellsAn IgG-like Domain in the Minor Pilin GBS52 of Streptococcus agalactiae Mediates Lung Epithelial Cell AdhesionIncreased Risk of Group B Streptococcus Invasive Infection in HIV-Exposed but Uninfected Infants: A Review of the Evidence and Possible MechanismsWhole-Genome Sequencing of Invasion-Resistant Cells Identifies Laminin α2 as a Host Factor for Bacterial InvasionThreonine phosphorylation prevents promoter DNA binding of the Group B Streptococcus response regulator CovR.Interactions of the streptococcal C5a peptidase with human fibronectin.Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid.Group B streptococcal beta-hemolysin/cytolysin directly impairs cardiomyocyte viability and functionExtensive adaptive changes occur in the transcriptome of Streptococcus agalactiae (group B streptococcus) in response to incubation with human blood.Functional characterization of a newly identified group B Streptococcus pullulanase eliciting antibodies able to prevent alpha-glucans degradation.Global transcriptional profiling reveals Streptococcus agalactiae genes controlled by the MtaR transcription factor.Siglec-5 and Siglec-14 are polymorphic paired receptors that modulate neutrophil and amnion signaling responses to group B Streptococcus.Two coregulated efflux transporters modulate intracellular heme and protoporphyrin IX availability in Streptococcus agalactiae.The 2-Cys peroxiredoxin alkyl hydroperoxide reductase c binds heme and participates in its intracellular availability in Streptococcus agalactiae.Computational bacterial genome-wide analysis of phylogenetic profiles reveals potential virulence genes of Streptococcus agalactiae.Emerging trends in invasive and noninvasive isolates of Streptococcus agalactiae in a Latin American hospital: a 17-year study.Inhibition of IL-10 production by maternal antibodies against Group B Streptococcus GAPDH confers immunity to offspring by favoring neutrophil recruitmentInteraction between pathogenic bacteria and intrauterine leukocytes triggers alternative molecular signaling cascades leading to labor in womenMechanisms of microbial escape from phagocyte killing.Prophagic DNA fragments in Streptococcus agalactiae strains and association with neonatal meningitis.Structural characterization of the virulence factor nuclease A from Streptococcus agalactiaeGranadaene: proposed structure of the group B Streptococcus polyenic pigment.Association and virulence gene expression vary among serotype III group B streptococcus isolates following exposure to decidual and lung epithelial cells.β-Hemolysin/cytolysin of Group B Streptococcus enhances host inflammation but is dispensable for establishment of urinary tract infection.Interaction of neonatal phagocytes with group B streptococcus: recognition and response.Group B Streptococcus hijacks the host plasminogen system to promote brain endothelial cell invasionNeonatal immune adaptation of the gut and its role during infections.Group B streptococcal haemolysin and pigment, a tale of twins.Loss of catabolic function in Streptococcus agalactiae strains and its association with neonatal meningitis.The sensor histidine kinase RgfC affects group B streptococcal virulence factor expression independent of its response regulator RgfA.Antimicrobial susceptibility profiles, serotype distribution and virulence determinants among invasive, non-invasive and colonizing Streptococcus agalactiae (group B streptococcus) from Malaysian patients.Immune activation and suppression by group B streptococcus in a murine model of urinary tract infectionMutation of the maturase lipoprotein attenuates the virulence of Streptococcus equi to a greater extent than does loss of general lipoprotein lipidationBacterial Pili exploit integrin machinery to promote immune activation and efficient blood-brain barrier penetration.Expression, purification, crystallization and preliminary X-ray diffraction studies of the human keratin 4-binding domain of serine-rich repeat protein 1 from Streptococcus agalactiae.Serine/threonine phosphatase Stp1 mediates post-transcriptional regulation of hemolysin, autolysis, and virulence of group B Streptococcus.Group B streptococcal capsular sialic acids interact with siglecs (immunoglobulin-like lectins) on human leukocytesEvaluation of the ability of Streptococcus agalactiae strains isolated from genital and neonatal specimens to bind to human fibrinogen and correlation with characteristics of the fbsA and fbsB genesIsolation and anti-microbial susceptibility pattern of group B Streptococcus among pregnant women attending antenatal clinics in Ayder Referral Hospital and Mekelle Health Center, Mekelle, Northern Ethiopia.Identification of CiaR Regulated Genes That Promote Group B Streptococcal Virulence and Interaction with Brain Endothelial Cells
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P2860
Molecular pathogenesis of neonatal group B streptococcal infection: no longer in its infancy.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
2004年论文
@zh
2004年论文
@zh-cn
name
Molecular pathogenesis of neon ...... ion: no longer in its infancy.
@ast
Molecular pathogenesis of neon ...... ion: no longer in its infancy.
@en
type
label
Molecular pathogenesis of neon ...... ion: no longer in its infancy.
@ast
Molecular pathogenesis of neon ...... ion: no longer in its infancy.
@en
prefLabel
Molecular pathogenesis of neon ...... ion: no longer in its infancy.
@ast
Molecular pathogenesis of neon ...... ion: no longer in its infancy.
@en
P1476
Molecular pathogenesis of neon ...... ion: no longer in its infancy.
@en
P2093
Kelly S Doran
P356
10.1111/J.1365-2958.2004.04266.X
P407
P50
P577
2004-10-01T00:00:00Z