Spermine causes loss of innate immune response to Helicobacter pylori by inhibition of inducible nitric-oxide synthase translation. - Wikidata - awgldk - TriplyDB

Spermine causes loss of innate immune response to Helicobacter pylori by inhibition of inducible nitric-oxide synthase translation.

Spermine causes loss of innate immune response to Helicobacter pylori by inhibition of inducible nitric-oxide synthase translation.

http://www.wikidata.org/entity/Q40490825

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Redox biology and gastric carcinogenesis: the role of Helicobacter pylori Arginine Metabolism in Bacterial Pathogenesis and Cancer Therapy Characterization and inactivation of an agmatine deiminase from Helicobacter pylori Integrated regulation of the type III secretion system and other virulence determinants in Ralstonia solanacearum Oxidative Stress Resulting From Helicobacter pylori Infection Contributes to Gastric Carcinogenesis.Modulation of the arginase pathway in the context of microbial pathogenesis: a metabolic enzyme moonlighting as an immune modulator Arginase II restricts host defense to Helicobacter pylori by attenuating inducible nitric oxide synthase translation in macrophages Inducible nitric oxide synthase polymorphism is associated with the increased risk of differentiated gastric cancer in a Japanese population Increased expression and cellular localization of spermine oxidase in ulcerative colitis and relationship to disease activity Cationic amino acid transporter 2 enhances innate immunity during Helicobacter pylori infection.Helicobacter pylori and gastric cancer: factors that modulate disease risk.L-arginine supplementation improves responses to injury and inflammation in dextran sulfate sodium colitis Polyamines Impair Immunity to Helicobacter pylori by Inhibiting L-Arginine Uptake Required for Nitric Oxide Production Role of innate immunity in Helicobacter pylori-induced gastric malignancy.Transcriptional profiling of gastric epithelial cells infected with wild type or arginase-deficient Helicobacter pylori.Toll-like receptor-induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens.Immune evasion by Helicobacter pylori is mediated by induction of macrophage arginase II Spermine reverses lipopolysaccharide-induced memory deficit in mice.Crystallization and preliminary crystallographic studies of Helicobacter pylori arginase Effect of arginase inhibition on pulmonary L-arginine metabolism in murine Pseudomonas pneumonia Arginine and polyamines in Helicobacter pylori-induced immune dysregulation and gastric carcinogenesis.Metabolism links bacterial biofilms and colon carcinogenesis.L-arginine and cationic amino acid transporter 2B regulate growth and survival of Leishmania amazonensis amastigotes in macrophages.L-arginine availability regulates inducible nitric oxide synthase-dependent host defense against Helicobacter pylori.L-arginine uptake by cationic amino acid transporter 2 is essential for colonic epithelial cell restitution.Helicobacter pylori and Gastric Malignancy.Genetic factors involved in the development of Helicobacter pylori-related gastric cancer.The apolipoprotein E-mimetic peptide COG112 inhibits the inflammatory response to Citrobacter rodentium in colonic epithelial cells by preventing NF-kappaB activation.The first description of complete invertebrate arginine metabolism pathways implies dose-dependent pathogen regulation in Apostichopus japonicus.Immunological research using RNA interference technology.The Immune Battle against Helicobacter pylori Infection: NO Offense.Pneumocystis mediates overexpression of antizyme inhibitor resulting in increased polyamine levels and apoptosis in alveolar macrophages.A multifaceted role for polyamines in bacterial pathogens.Spermine oxidase is a regulator of macrophage host response to Helicobacter pylori: enhancement of antimicrobial nitric oxide generation by depletion of spermine Arginase: an emerging key player in the mammalian immune system.Streptococcus pyogenes arginine and citrulline catabolism promotes infection and modulates innate immunity.Metabolism via Arginase or Nitric Oxide Synthase: Two Competing Arginine Pathways in Macrophages Dual role of arginine metabolism in establishing pathogenesis.Changes in the proteomic profile during the differential polarization status of the human monocyte-derived macrophage THP-1 cell line.Arginine Metabolism in Myeloid Cells Shapes Innate and Adaptive Immunity.

P2860

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P2860

Spermine causes loss of innate immune response to Helicobacter pylori by inhibition of inducible nitric-oxide synthase translation.

http://www.wikidata.org/entity/Q40490825

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Spermine causes loss of innate ...... ic-oxide synthase translation.

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Alain P Gobert

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Amy Hacker

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Darren R Blumberg

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Françoise I Bussière

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Hangxiu Xu

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Mohammad Asim

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Preston Y Kim

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Robert A Casero

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Rupesh Chaturvedi

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Yulan Cheng

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P2860

Identification and characterization of a novel flavin-containing spermine oxidase of mammalian cell origin

Nitric oxide and macrophage function

Spermine oxidation induced by Helicobacter pylori results in apoptosis and DNA damage: implications for gastric carcinogenesis.

Translational regulation of ornithine decarboxylase and other enzymes of the polyamine pathway.

Helicobacter pylori arginase inhibits nitric oxide production by eukaryotic cells: a strategy for bacterial survival

The mechanism of the inhibitory effect of polyamines on the induction of nitric oxide synthase: role of aldehyde metabolites.

Translational control of inducible nitric oxide synthase expression by arginine can explain the arginine paradox.

The role of polyamine catabolism in anti-tumour drug response.

Soluble surface proteins from Helicobacter pylori activate monocytes/macrophages by lipopolysaccharide-independent mechanism.

Surface proteins from Helicobacter pylori exhibit chemotactic activity for human leukocytes and are present in gastric mucosa.

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Helicobacter pylori