Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
about
Arginase: a key enzyme in the pathophysiology of allergic asthma opening novel therapeutic perspectivesOxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammationIL-4 dependent alternatively-activated macrophages have a distinctive in vivo gene expression phenotypeCytokine and Growth Factor Activation In Vivo and In Vitro after Spinal Cord InjuryMyeloid-Derived Suppressor Cells in Bacterial InfectionsMacrophage Bactericidal Activities against Staphylococcus aureus Are Enhanced In Vivo by Selenium Supplementation in a Dose-Dependent MannerAntibodies trap tissue migrating helminth larvae and prevent tissue damage by driving IL-4Rα-independent alternative differentiation of macrophagesChitinase dependent control of protozoan cyst burden in the brainLong-Term Relationships: the Complicated Interplay between the Host and the Developmental Stages of Toxoplasma gondii during Acute and Chronic InfectionsEbola: translational science considerationsMyeloid-derived suppressor cells as regulators of the immune systemArginase and pulmonary diseasesReprogramming of lysosomal gene expression by interleukin-4 and Stat6Role of nod2 in the response of macrophages to toll-like receptor agonistsMacrophage-specific PPARgamma controls alternative activation and improves insulin resistanceProtective and pathogenic functions of macrophage subsetsMacrophage activation and polarization: nomenclature and experimental guidelinesFatal outcome of pandemic H1N1 2009 influenza virus infection is associated with immunopathology and impaired lung repair, not enhanced viral burden, in pregnant miceMyeloid-derived suppressor cells: the dark knight or the joker in viral infections?Sphingosine-1-phosphate induces an antiinflammatory phenotype in macrophages.Alterations of the arginine metabolome in asthma.Neurological and behavioral abnormalities, ventricular dilatation, altered cellular functions, inflammation, and neuronal injury in brains of mice due to common, persistent, parasitic infection.Ca2+/calmodulin-dependent kinase kinase alpha is expressed by monocytic cells and regulates the activation profile.Cationic amino acid transporter-2 regulates immunity by modulating arginase activity.Bone marrow cell derived arginase I is the major source of allergen-induced lung arginase but is not required for airway hyperresponsiveness, remodeling and lung inflammatory responses in mice.Arginase II restricts host defense to Helicobacter pylori by attenuating inducible nitric oxide synthase translation in macrophagesHelminth regulation of host IL-4Ralpha/Stat6 signaling: mechanism underlying NOS-2 inhibition by Trichinella spiralisControl of macrophage activation and function by PPARs.Toxoplasma gondii rhoptry kinase ROP16 activates STAT3 and STAT6 resulting in cytokine inhibition and arginase-1-dependent growth controlToll-like receptors 2 and 4 regulate the frequency of IFNγ-producing CD4+ T-cells during pulmonary infection with Chlamydia pneumoniaeArginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signalingMetallomic analysis of macrophages infected with Histoplasma capsulatum reveals a fundamental role for zinc in host defenses.Progressive visceral leishmaniasis is driven by dominant parasite-induced STAT6 activation and STAT6-dependent host arginase 1 expression.Aberrant host defense against Leishmania major in the absence of SLPI.Functions of arginase isoforms in macrophage inflammatory responses: impact on cardiovascular diseases and metabolic disorders.Tumor induced hepatic myeloid derived suppressor cells can cause moderate liver damage.Genetic polymorphisms in arginase I and II and childhood asthma and atopyCurrent status of immune mechanisms of killing of intracellular microorganisms.Arginase 1 overexpression in psoriasis: limitation of inducible nitric oxide synthase activity as a molecular mechanism for keratinocyte hyperproliferation.Toll-like receptor-induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens.
P2860
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P2860
Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
description
2001 nî lūn-bûn
@nan
2001 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
@ast
Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
@en
type
label
Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
@ast
Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
@en
prefLabel
Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
@ast
Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
@en
P2093
P1476
Cutting edge: Stat6-dependent substrate depletion regulates nitric oxide production.
@en
P2093
P304
P356
10.4049/JIMMUNOL.166.4.2173
P407
P577
2001-02-01T00:00:00Z