Clostridium sordellii lethal toxin kills mice by inducing a major increase in lung vascular permeability - Wikidata - awgldk - TriplyDB

Clostridium sordellii lethal toxin kills mice by inducing a major increase in lung vascular permeability

Clostridium sordellii lethal toxin kills mice by inducing a major increase in lung vascular permeability

http://www.wikidata.org/entity/Q35781403

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Lethal toxin is a critical determinant of rapid mortality in rodent models of Clostridium sordellii endometritis.Diet-induced alterations in gut microflora contribute to lethal pulmonary damage in TLR2/TLR4-deficient mice.Perivascular fluid cuffs decrease lung compliance by increasing tissue resistance.Comparative analysis of the extracellular proteomes of two Clostridium sordellii strains exhibiting contrasting virulence Bacterial factors exploit eukaryotic Rho GTPase signaling cascades to promote invasion and proliferation within their host.TcsL is an essential virulence factor in Clostridium sordellii ATCC 9714 Tissue expression of steroid hormone receptors is associated with differential immune responsiveness.Foot infection by Clostridium sordellii: case report and review of 15 cases in France.Non-toxigenic Clostridium sordellii: clinical and microbiological features of a case of cholangitis-associated bacteremia.A novel murine model of Clostridium sordellii myonecrosis: Insights into the pathogenesis of disease Clostridium sordellii Lethal-Toxin Autoprocessing and Membrane Localization Activities Drive GTPase Glucosylation Profiles in Endothelial Cells.The Sialidase NanS Enhances Non-TcsL Mediated Cytotoxicity of Clostridium sordellii Fatal Spontaneous Clostridium bifermentans Necrotizing Endometritis: A Case Report and Literature Review of the Pathogen.Clostridial toxins.Experimental identification and computational characterization of a novel extracellular metalloproteinase produced by Clostridium sordellii.Gynecologic clostridial toxic shock in women of reproductive age.Bacterial toxins and the nervous system: neurotoxins and multipotential toxins interacting with neuronal cells.Development of ELISA based detection system for lethal toxin of Clostridium sordellii.Haemorrhagic toxin and lethal toxin from Clostridium sordellii strain vpi9048: molecular characterization and comparative analysis of substrate specificity of the large clostridial glucosylating toxins.Clostridium sordellii Pathogenicity Locus Plasmid pCS1-1 Encodes a Novel Clostridial Conjugation Locus.

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Clostridium sordellii lethal toxin kills mice by inducing a major increase in lung vascular permeability

http://www.wikidata.org/entity/Q35781403

description

2007 nî lūn-bûn

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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2007年论文

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2007年论文

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name

Clostridium sordellii lethal t ...... in lung vascular permeability

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Clostridium sordellii lethal t ...... in lung vascular permeability

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Clostridium sordellii lethal t ...... in lung vascular permeability

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Clostridium sordellii lethal t ...... in lung vascular permeability

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Clostridium sordellii lethal t ...... in lung vascular permeability

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Clostridium sordellii lethal t ...... in lung vascular permeability

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The American Journal of Pathology

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Clostridium sordellii lethal t ...... in lung vascular permeability

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Blandine Geny

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Catherine Fitting

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Leticia Zarantonelli

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Marek Szatanik

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Marie-Christine Prevost

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Michel R Popoff

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Nadège Cayet

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P2860

Role of phosphoinositide 3-OH kinase in cell transformation and control of the actin cytoskeleton by Ras

Corticotropin-releasing hormone (CRH) requirement in Clostridium difficile toxin A-mediated intestinal inflammation

Anthrax lethal factor cleaves MKK3 in macrophages and inhibits the LPS/IFNgamma-induced release of NO and TNFalpha

Rho GTPases and their effector proteins

The many roles of chemokines and chemokine receptors in inflammation

Clostridium difficile toxin B is an inflammatory enterotoxin in human intestine.

Cellular uptake of Clostridium difficile toxin B. Translocation of the N-terminal catalytic domain into the cytosol of eukaryotic cells.

Requirement of Rac activity for maintenance of capillary endothelial barrier properties.

Nitric oxide and nitrotyrosine in the lungs of patients with acute respiratory distress syndrome.

Regulation of cadherin-mediated cell-cell adhesion by the Rho family GTPases.

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1003-1017

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10.2353/AJPATH.2007.060583

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Christelle Mazuet

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6484657

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