Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes. - Test2 - elhamkhani - TriplyDB

Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes.

Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes.

http://www.wikidata.org/entity/Q40057699

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Monoamine oxidases (MAO) in the pathogenesis of heart failure and ischemia/reperfusion injury Novel Perspectives in Redox Biology and Pathophysiology of Failing Myocytes: Modulation of the Intramyocardial Redox Milieu for Therapeutic Interventions-A Review Article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology Diabetic Cardiovascular Disease Induced by Oxidative Stress The balance of powers: Redox regulation of fibrogenic pathways in kidney injury Endoplasmic reticulum stress and Nox-mediated reactive oxygen species signaling in the peripheral vasculature: potential role in hypertension Abnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balance Evolution of NADPH Oxidase Inhibitors: Selectivity and Mechanisms for Target Engagement Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning Atrial fibrillation therapy now and in the future: drugs, biologicals, and ablation New insights into the role of mitochondrial dynamics and autophagy during oxidative stress and aging in the heart Biochemistry, physiology, and pathophysiology of NADPH oxidases in the cardiovascular system Redox modification of cell signaling in the cardiovascular system NADPH oxidases in heart failure: poachers or gamekeepers?Mitochondria as a therapeutic target in heart failure Heart failure and mitochondrial dysfunction: the role of mitochondrial fission/fusion abnormalities and new therapeutic strategies Mitochondria and cardiovascular aging Regulation of cell survival and death by pyridine nucleotides Physiological and pathological functions of NADPH oxidases during myocardial ischemia-reperfusion NADPH oxidases in lung health and disease The role of sirtuins in cardiac disease Molecular targeting of NOX4 for neuropathic pain after traumatic injury of the spinal cord.Redox regulation of mitochondrial function Cross talk between mitochondria and NADPH oxidases Oxidases and peroxidases in cardiovascular and lung disease: new concepts in reactive oxygen species signaling Reactive oxygen species in inflammation and tissue injury Mitochondrial redox signaling: Interaction of mitochondrial reactive oxygen species with other sources of oxidative stress CRISPR-Cas9 Mediated NOX4 Knockout Inhibits Cell Proliferation and Invasion in HeLa Cells Reactive Oxygen Species/Nitric Oxide Mediated Inter-Organ Communication in Skeletal Muscle Wasting Diseases.The liver-specific tumor suppressor STAT5 controls expression of the reactive oxygen species-generating enzyme NOX4 and the proapoptotic proteins PUMA and BIM in mice.Wild-type and mutant p53 differentially regulate NADPH oxidase 4 in TGF-β-mediated migration of human lung and breast epithelial cells NADPH oxidases: a perspective on reactive oxygen species production in tumor biology Role of NAD(P)H oxidase in superoxide generation and endothelial dysfunction in Goto-Kakizaki (GK) rats as a model of nonobese NIDDM.Parkin regulation of CHOP modulates susceptibility to cardiac endoplasmic reticulum stress.Whole transcriptome analysis of the fasting and fed Burmese python heart: insights into extreme physiological cardiac adaptation NADPH Oxidases: Insights into Selected Functions and Mechanisms of Action in Cancer and Stem Cells.Mitochondria and ageing: role in heart, skeletal muscle and adipose tissue.Mst1 promotes cardiac myocyte apoptosis through phosphorylation and inhibition of Bcl-xL The Role of NOX4 and TRX2 in Angiogenesis and Their Potential Cross-Talk.NADPH oxidase 4 induces cardiac arrhythmic phenotype in zebrafish Divergent molecular mechanisms underlying the pleiotropic functions of macrophage inhibitory cytokine-1 in cancer

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P2860

Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes.

http://www.wikidata.org/entity/Q40057699

description

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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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2010年論文

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2010年论文

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2010年论文

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2010年论文

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name

Upregulation of Nox4 by hypert ...... sfunction in cardiac myocytes.

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type

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Upregulation of Nox4 by hypert ...... sfunction in cardiac myocytes.

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Upregulation of Nox4 by hypert ...... sfunction in cardiac myocytes.

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CIRCRESAHA.109.213116

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Circulation Research

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Upregulation of Nox4 by hypert ...... ysfunction in cardiac myocytes

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Cexiong Fu

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Hong Li

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Jayashree Pain

http://www.w3.org/2001/XMLSchema#string

Junya Kuroda

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P2860

The NAD(P)H oxidase homolog Nox4 modulates insulin-stimulated generation of H2O2 and plays an integral role in insulin signal transduction

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

Functional analysis of Nox4 reveals unique characteristics compared to other NADPH oxidases

Direct interaction of the novel Nox proteins with p22phox is required for the formation of a functionally active NADPH oxidase

Structure, regulation and evolution of Nox-family NADPH oxidases that produce reactive oxygen species

Subcellular localization of Nox4 and regulation in diabetes

Reversible redox-dependent modulation of mitochondrial aconitase and proteolytic activity during in vivo cardiac ischemia/reperfusion

Mitochondria, oxidants, and aging

The NADPH oxidase Nox3 constitutively produces superoxide in a p22phox-dependent manner: its regulation by oxidase organizers and activators.

A novel superoxide-producing NAD(P)H oxidase in kidney.

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1253-1264

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10.1161/CIRCRESAHA.109.213116

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7

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106

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Junichi Sadoshima

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2010-02-25T00:00:00Z

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20185797

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2855780

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