Regulation of CovR expression in Group B Streptococcus impacts blood-brain barrier penetration. - Wikidata - wikimedia - TriplyDB

Regulation of CovR expression in Group B Streptococcus impacts blood-brain barrier penetration.

Regulation of CovR expression in Group B Streptococcus impacts blood-brain barrier penetration.

http://www.wikidata.org/entity/Q29346580

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Defense at the border: the blood-brain barrier versus bacterial foreigners A streptococcal lipid toxin induces membrane permeabilization and pyroptosis leading to fetal injury A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta Adaptive response of Group B streptococcus to high glucose conditions: new insights on the CovRS regulation network The Abi-domain protein Abx1 interacts with the CovS histidine kinase to control virulence gene expression in group B Streptococcus.Dual-site phosphorylation of the control of virulence regulator impacts group a streptococcal global gene expression and pathogenesis Group B Streptococcus interactions with human meningeal cells and astrocytes in vitro.Interaction of Streptococcus agalactiae and Cellular Innate Immunity in Colonization and Disease Infection of human coronary artery endothelial cells by group B streptococcus contributes to dysregulation of apoptosis, hemostasis, and innate immune responses The role of autophagy during group B Streptococcus infection of blood-brain barrier endothelium Group B streptococcal haemolysin and pigment, a tale of twins.The sensor histidine kinase RgfC affects group B streptococcal virulence factor expression independent of its response regulator RgfA.Streptococcus agalactiae infection in zebrafish larvae Serine/threonine protein kinase Stk is required for virulence, stress response, and penicillin tolerance in Streptococcus pyogenes.Contribution of lethal toxin and edema toxin to the pathogenesis of anthrax meningitis.Bacterial Pili exploit integrin machinery to promote immune activation and efficient blood-brain barrier penetration.Aspects of eukaryotic-like signaling in Gram-positive cocci: a focus on virulence.Serine/threonine phosphatase Stp1 mediates post-transcriptional regulation of hemolysin, autolysis, and virulence of group B Streptococcus.Bacterial induction of Snail1 contributes to blood-brain barrier disruption.Identification of CiaR Regulated Genes That Promote Group B Streptococcal Virulence and Interaction with Brain Endothelial Cells Mast cell degranulation by a hemolytic lipid toxin decreases GBS colonization and infection Regulation of PI-2b Pilus Expression in Hypervirulent Streptococcus agalactiae ST-17 BM110.CsrRS and environmental pH regulate group B streptococcus adherence to human epithelial cells and extracellular matrix Molecular Characterization of Nonhemolytic and Nonpigmented Group B Streptococci Responsible for Human Invasive Infections.Group B Streptococcus CovR regulation modulates host immune signalling pathways to promote vaginal colonization Concepts and mechanisms: crossing host barriers.The two-component response regulator LiaR regulates cell wall stress responses, pili expression and virulence in group B Streptococcus.Group B Streptococcus circumvents neutrophils and neutrophil extracellular traps during amniotic cavity invasion and preterm labor.BsaB, a novel adherence factor of group B Streptococcus.Regulation of prokaryotic gene expression by eukaryotic-like enzymes.The CovS/CovR acid response regulator is required for intracellular survival of group B Streptococcus in macrophages.PbsP, a cell wall-anchored protein that binds plasminogen to promote hematogenous dissemination of group B Streptococcus.Mast Cell Chymase Decreases The Severity Of Group B Streptococcus Infections.Quantitative assessment of the blood-brain barrier opening caused by Streptococcus agalactiae hyaluronidase in a BALB/c mouse model.A phosphoramidon-sensitive metalloprotease induces apoptosis of human endothelial cells by Group B Streptococcus.Modeling Group B Streptococcus and Blood-Brain Barrier Interaction by Using Induced Pluripotent Stem Cell-Derived Brain Endothelial Cells.Diminished capsule exacerbates virulence, blood brain barrier penetration, intracellular persistence and antibiotic evasion of hyperhemolytic Group B Streptococcus.A non-hemolytic Group B Streptococcus strain exhibits hypervirulence.Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches.Characterization of a two-component system transcriptional regulator LtdR that impacts Group B Streptococcal colonization and disease.

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Regulation of CovR expression in Group B Streptococcus impacts blood-brain barrier penetration.

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2010年の論文

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Regulation of CovR expression ...... ood-brain barrier penetration.

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Regulation of CovR expression ...... ood-brain barrier penetration.

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Regulation of CovR expression ...... ood-brain barrier penetration.

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Regulation of CovR expression ...... ood-brain barrier penetration.

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Regulation of CovR expression ...... ood-brain barrier penetration.

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Molecular Microbiology

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Regulation of CovR expression ...... ood-brain barrier penetration.

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Anirban Banerjee

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Annalisa Lembo

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Anthony Vo

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Christian W Renken

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James E Connelly

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Kellie Burnside

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Kelly S Doran

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Lakshmi Rajagopal

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Melissa de los Reyes

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P2860

Genome analysis of multiple pathogenic isolates of Streptococcus agalactiae: implications for the microbial "pan-genome"

Invasion of brain microvascular endothelial cells by group B streptococci

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

Two-component signal transduction

Understanding the regulation of Group B Streptococcal virulence factors

Recent advances in understanding the molecular basis of group B Streptococcus virulence

Threonine phosphorylation prevents promoter DNA binding of the Group B Streptococcus response regulator CovR.

CovS/CovR of group B streptococcus: a two-component global regulatory system involved in virulence.

rgf encodes a novel two-component signal transduction system of Streptococcus agalactiae.

Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid.

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10.1111/J.1365-2958.2010.07215.X

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2

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44625402

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20497331

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blood–brain barrier

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