Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis. - Wikidata - wikimedia - TriplyDB

Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis.

Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis.

http://www.wikidata.org/entity/Q34281699

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NADPH oxidase as a therapeutic target for oxalate induced injury in kidneys Subversion of host recognition and defense systems by Francisella spp A 14.7 kDa protein from Francisella tularensis subsp. novicida (named FTN_1133), involved in the response to oxidative stress induced by organic peroxides, is not endowed with thiol-dependent peroxidase activity Assembly of NADPH oxidase in human neutrophils is modulated by the opacity-associated protein expression State of Neisseria gonorrhoeae Influence of Microbes on Neutrophil Life and Death.Role of NK cells in host defense against pulmonary type A Francisella tularensis infection Macrophage replication screen identifies a novel Francisella hydroperoxide resistance protein involved in virulence.Host-pathogen interactions and immune evasion strategies in Francisella tularensis pathogenicity Differential expression of microRNAs in Francisella tularensis-infected human macrophages: miR-155-dependent downregulation of MyD88 inhibits the inflammatory response.Identification of disulfide bond isomerase substrates reveals bacterial virulence factors.Type A Francisella tularensis acid phosphatases contribute to pathogenesis.Regulation of francisella tularensis virulence.The francisella intracellular life cycle: toward molecular mechanisms of intracellular survival and proliferation.The subversion of the immune system by francisella tularensis.Phagocytic receptors dictate phagosomal escape and intracellular proliferation of Francisella tularensis.Immunofluorescence and confocal microscopy of neutrophils.The acid phosphatase AcpA is secreted in vitro and in macrophages by Francisella spp.Francisella tularensis inhibits the intrinsic and extrinsic pathways to delay constitutive apoptosis and prolong human neutrophil lifespan.Natural IgM mediates complement-dependent uptake of Francisella tularensis by human neutrophils via complement receptors 1 and 3 in nonimmune serum.Disruption of Francisella tularensis Schu S4 iglI, iglJ, and pdpC genes results in attenuation for growth in human macrophages and in vivo virulence in mice and reveals a unique phenotype for pdpC.Francisella tularensis Modulates a Distinct Subset of Regulatory Factors and Sustains Mitochondrial Integrity to Impair Human Neutrophil Apoptosis.Mechanisms of Francisella tularensis intracellular pathogenesis.Francisella tularensis alters human neutrophil gene expression: insights into the molecular basis of delayed neutrophil apoptosis.Possible links between stress defense and the tricarboxylic acid (TCA) cycle in Francisella pathogenesis.Neutrophils: potential therapeutic targets in tularemia?Glutamate utilization couples oxidative stress defense and the tricarboxylic acid cycle in Francisella phagosomal escape.A Francisella virulence factor catalyses an essential reaction of biotin synthesis.T-bet regulates immunity to Francisella tularensis live vaccine strain infection, particularly in lungs.TolC-dependent modulation of host cell death by the Francisella tularensis live vaccine strain.Immunity to Francisella.Oxidative and nitrosative stress on phagocytes' function: from effective defense to immunity evasion mechanisms.Proteins involved in Francisella tularensis survival and replication inside macrophages.Monocyte/macrophage inflammatory response pathways to combat Francisella infection: possible therapeutic targets?Regulation of human neutrophil apoptosis and lifespan in health and disease.Differential Growth of Francisella tularensis, Which Alters Expression of Virulence Factors, Dominant Antigens, and Surface-Carbohydrate Synthases, Governs the Apparent Virulence of Ft SchuS4 to Immunized Animals.Contribution of methionine sulfoxide reductase B (MsrB) to Francisella tularensis infection in mice.Francisella novicida inhibits spontaneous apoptosis and extends human neutrophil lifespan.Multifaceted effects of Francisella tularensis on human neutrophil function and lifespan.Neutrophils to the ROScue: Mechanisms of NADPH Oxidase Activation and Bacterial Resistance.Increased Resistance to Intradermal Francisella tularensis LVS Infection by Inactivation of the Sts Phosphatases.

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P2860

Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis.

http://www.wikidata.org/entity/Q34281699

description

2010 nî lūn-bûn

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2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2010 թվականի հուլիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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name

Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis.

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Journal of Leukocyte Biology

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Multiple mechanisms of NADPH o ...... type B Francisella tularensis

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P2093

Jessica G Moreland

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Justin T Schwartz

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Ramona L McCaffrey

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Stephen R Lindemann

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P2860

Protein secretion systems in bacterial-host associations, and their description in the Gene Ontology

Anion channels, including ClC-3, are required for normal neutrophil oxidative function, phagocytosis, and transendothelial migration

Comparative genomic characterization of Francisella tularensis strains belonging to low and high virulence subspecies

The bacterial type VI secretion machine: yet another player for protein transport across membranes

The phosphorylation of the respiratory burst oxidase component p47phox during neutrophil activation. Phosphorylation of sites recognized by protein kinase C and by proline-directed kinases

The role of protein kinase C in cell surface signal transduction and tumour promotion

Arachidonic acid and phosphorylation synergistically induce a conformational change of p47phox to activate the phagocyte NADPH oxidase.

The Francisella tularensis pathogenicity island encodes a secretion system that is required for phagosome escape and virulence.

Construction of a Francisella tularensis two-dimensional electrophoresis protein database.

Identification of fevR, a novel regulator of virulence gene expression in Francisella novicida.

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791-805

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10.1189/JLB.1209811

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4

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88

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Lee-Ann H Allen

Blake W. Buchan

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2010-07-07T00:00:00Z

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45101687

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20610796

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2974429

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