NADPH oxidase is required for the sensory plasticity of the carotid body by chronic intermittent hypoxia. - Wikidata - awgldk - TriplyDB

NADPH oxidase is required for the sensory plasticity of the carotid body by chronic intermittent hypoxia.

NADPH oxidase is required for the sensory plasticity of the carotid body by chronic intermittent hypoxia.

http://www.wikidata.org/entity/Q37217629

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Epigenetic Regulation of Carotid Body Oxygen Sensing: Clinical Implications Physiology in medicine: obstructive sleep apnea pathogenesis and treatment--considerations beyond airway anatomy Peripheral chemoreception and arterial pressure responses to intermittent hypoxia Pathogenic roles of the carotid body inflammation in sleep apnea Hypoxia-inducible factors and hypertension: lessons from sleep apnea syndrome Carotid body chemoreceptors, sympathetic neural activation, and cardiometabolic disease Neural Control of Blood Pressure in Chronic Intermittent Hypoxia Modulation of chronic hypoxia-induced chemoreceptor hypersensitivity by NADPH oxidase subunits in rat carotid body Upregulation of a local renin-angiotensin system in the rat carotid body during chronic intermittent hypoxia Hypoxia-inducible factor 1 mediates increased expression of NADPH oxidase-2 in response to intermittent hypoxia NADPH Oxidase-Derived ROS Induced by Chronic Intermittent Hypoxia Mediates Hypersensitivity of Lung Vagal C Fibers in Rats Effect of AT1 receptor blockade on intermittent hypoxia-induced endothelial dysfunction.Chronic intermittent hypoxia augments chemoreflex control of sympathetic activity: role of the angiotensin II type 1 receptor.Long-term effects of recurrent intermittent hypoxia and hyperoxia on respiratory system mechanics in neonatal mice.Neither serotonin nor adenosine-dependent mechanisms preserve ventilatory capacity in ALS rats Is insulin the new intermittent hypoxia?Pattern-specific sustained activation of tyrosine hydroxylase by intermittent hypoxia: role of reactive oxygen species-dependent downregulation of protein phosphatase 2A and upregulation of protein kinases H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea.Neonatal intermittent hypoxia impairs neuronal nicotinic receptor expression and function in adrenal chromaffin cells.Endothelin 1-dependent neurovascular dysfunction in chronic intermittent hypoxia.Carotid body, insulin, and metabolic diseases: unraveling the links.NADPH oxidase 2 mediates intermittent hypoxia-induced mitochondrial complex I inhibition: relevance to blood pressure changes in rats Mechanisms of sympathetic activation and blood pressure elevation by intermittent hypoxia Intermittent hypoxia augments acute hypoxic sensing via HIF-mediated ROS Enhanced carotid body chemosensory activity and the cardiovascular alterations induced by intermittent hypoxia Enhanced neuropeptide Y synthesis during intermittent hypoxia in the rat adrenal medulla: role of reactive oxygen species-dependent alterations in precursor peptide processing Reactive oxygen species and the brain in sleep apnea.CaV3.2 T-type Ca²⁺ channels in H₂S-mediated hypoxic response of the carotid body.Chronic intermittent hypoxia increases rat sternohyoid muscle NADPH oxidase expression with attendant modest oxidative stress.HIF-1α activation by intermittent hypoxia requires NADPH oxidase stimulation by xanthine oxidase Sensory plasticity of the carotid body: role of reactive oxygen species and physiological significance.Adenosine A₂a receptors and O₂ sensing in development Angiotensin II evokes sensory long-term facilitation of the carotid body via NADPH oxidase.Hydrogen peroxide differentially affects activity in the pre-Bötzinger complex and hippocampus Nitric Oxide Bioavailability in Obstructive Sleep Apnea: Interplay of Asymmetric Dimethylarginine and Free Radicals.Regulation of carotid body oxygen sensing by hypoxia-inducible factors The NOX toolbox: validating the role of NADPH oxidases in physiology and disease.Metabolic dysfunction in obstructive sleep apnea: A critical examination of underlying mechanisms Carotid chemoreceptor development in mice Sympatho-adrenal activation by chronic intermittent hypoxia.

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NADPH oxidase is required for the sensory plasticity of the carotid body by chronic intermittent hypoxia.

http://www.wikidata.org/entity/Q37217629

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on April 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

NADPH oxidase is required for ...... chronic intermittent hypoxia.

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NADPH oxidase is required for ...... chronic intermittent hypoxia.

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type

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NADPH oxidase is required for ...... chronic intermittent hypoxia.

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NADPH oxidase is required for ...... chronic intermittent hypoxia.

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NADPH oxidase is required for ...... chronic intermittent hypoxia.

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NADPH oxidase is required for ...... chronic intermittent hypoxia.

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JNEUROSCI.4768-08.2009

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Journal of Neuroscience

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NADPH oxidase is required for ...... y chronic intermittent hypoxia

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E Deneris

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G K Kumar

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G Yuan

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J Nanduri

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N R Prabhakar

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N Wang

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S Pendyala

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V Natarajan

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P2860

Cell transformation by the superoxide-generating oxidase Mox1

A mammalian H+ channel generated through alternative splicing of the NADPH oxidase homolog NOH-1

The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology

The ETS domain factor Pet-1 is an early and precise marker of central serotonin neurons and interacts with a conserved element in serotonergic genes

Elevated glucose and diabetes promote interleukin-12 cytokine gene expression in mouse macrophages.

Role of Nox4 and Nox2 in hyperoxia-induced reactive oxygen species generation and migration of human lung endothelial cells.

Oxygen sensing by the carotid body chemoreceptors.

Pet-1 ETS gene plays a critical role in 5-HT neuron development and is required for normal anxiety-like and aggressive behavior.

Respiratory plasticity: differential actions of continuous and episodic hypoxia and hypercapnia.

Synaptic plasticity deficits and mild memory impairments in mouse models of chronic granulomatous disease.

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10.1523/JNEUROSCI.4768-08.2009

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24280620

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