The large-conductance Ca2+-activated K+ channel is essential for innate immunity. - Wikidata - awgldk - TriplyDB

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

http://www.wikidata.org/entity/Q34301370

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Chronic Granulomatous Disease; fundamental stages in our understanding of CGD The voltage-gated potassium channel Kv1.3 is highly expressed on inflammatory infiltrates in multiple sclerosis brain Apolipoprotein B Is an innate barrier against invasive Staphylococcus aureus infection Special article: chronic granulomatous disease in the United Kingdom and Ireland: a comprehensive national patient-based registry How neutrophils kill microbes What really happens in the neutrophil phagosome?Hypoxia and ischemia-reperfusion: a BiK contribution?How do microbes evade neutrophil killing?Splicing of the rSlo gene affects the molecular composition and drug response of Ca2+-activated K+ channels in skeletal muscle Up-Regulatory Effects of Curcumin on Large Conductance Ca2+-Activated K+ Channels BK channels in innate immune functions of neutrophils and macrophages.A role for BK channels in heart rate regulation in rodents VSOP/Hv1 proton channels sustain calcium entry, neutrophil migration, and superoxide production by limiting cell depolarization and acidification.Big Potassium (BK) ion channels in biology, disease and possible targets for cancer immunotherapy.Increasing reactive oxygen species as a therapeutic approach to treat hereditary leiomyomatosis and renal cell carcinoma Roles of the host oxidative immune response and bacterial antioxidant rubrerythrin during Porphyromonas gingivalis infection.Electron and proton transport by NADPH oxidases Tuning magnesium sensitivity of BK channels by mutations.SK channels mediate NADPH oxidase-independent reactive oxygen species production and apoptosis in granulocytes.Neutrophil antimicrobial defense against Staphylococcus aureus is mediated by phagolysosomal but not extracellular trap-associated cathelicidin.During the respiratory burst, do phagocytes need proton channels or potassium channels, or both?The NADPH oxidase of professional phagocytes--prototype of the NOX electron transport chain systems.Distinct endocytic mechanisms of CD22 (Siglec-2) and Siglec-F reflect roles in cell signaling and innate immunity.Large conductance, calcium- and voltage-gated potassium (BK) channels: regulation by cholesterol.Taming the neutrophil: calcium clearance and influx mechanisms as novel targets for pharmacological control.Streptolysin O Rapidly Impairs Neutrophil Oxidative Burst and Antibacterial Responses to Group A Streptococcus.MaxiK channel partners: physiological impact.Effects of multiple metal binding sites on calcium and magnesium-dependent activation of BK channels The antibacterial activity of human neutrophils and eosinophils requires proton channels but not BK channels Modulation of the conductance-voltage relationship of the BK Ca channel by mutations at the putative flexible interface between two RCK domains.Consequences of the electrogenic function of the phagocytic NADPH oxidase.The NH2 terminus of RCK1 domain regulates Ca2+-dependent BK(Ca) channel gating.Enhanced killing of intracellular multidrug-resistant Mycobacterium tuberculosis by compounds that affect the activity of efflux pumps.The function of the NADPH oxidase of phagocytes and its relationship to other NOXs in plants, invertebrates, and mammals.Activation of antibacterial autophagy by NADPH oxidases.Hv1 proton channels are required for high-level NADPH oxidase-dependent superoxide production during the phagocyte respiratory burst K+ channel modulators for the treatment of neurological disorders and autoimmune diseases Defective organellar acidification as a cause of cystic fibrosis lung disease: reexamination of a recurring hypothesis.NADPH oxidase-4 mediates myofibroblast activation and fibrogenic responses to lung injury.The role of nitrite ion in phagocyte function--perspectives and puzzles.

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P2860

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

http://www.wikidata.org/entity/Q34301370

description

2004 nî lūn-bûn

@nan

2004 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2004 թվականի փետրվարին հրատարակված գիտական հոդված

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2004年の論文

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2004年論文

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2004年論文

@zh-hant

2004年論文

@zh-hk

2004年論文

@zh-mo

2004年論文

@zh-tw

2004年论文

@wuu

name

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@ast

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@en

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@nl

type

label

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@ast

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@en

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@nl

prefLabel

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@ast

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@en

The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

@nl

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The large-conductance Ca2+-activated K+ channel is essential for innate immunity.

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P2093

Andrew Tinker

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Jatinder Ahluwalia

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Muriel Nobles

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P2860

Killing activity of neutrophils is mediated through activation of proteases by K+ flux

Maxi K+ channel mediates regulatory volume decrease response in a human bronchial epithelial cell line

Purification and characterization of a unique, potent, peptidyl probe for the high conductance calcium-activated potassium channel from venom of the scorpion Buthus tamulus

The effects of intracellular pH changes on resting cytosolic calcium in voltage-clamped snail neurones

Exploration of the role of reactive oxygen species in glutamate neurotoxicity in rat hippocampal neurones in culture

Activation of NADPH oxidase-related proton and electron currents in human eosinophils by arachidonic acid

The endocannabinoid anandamide is a direct and selective blocker of the background K(+) channel TASK-1.

Potassium channel openers as potential therapeutic weapons in ion channel disease.

Phagocytes and oxidative stress.

High-conductance calcium-activated potassium channels; structure, pharmacology, and function.

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853-858

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scholarly article

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10.1038/NATURE02356

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6977

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427

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Michael R. Duchen

Andrey Y Abramov

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2004-02-01T00:00:00Z

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8683648

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1041937350

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14985765

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2099462

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