Ca2+/Calmodulin-dependent protein kinase II δ mediates myocardial ischemia/reperfusion injury through nuclear factor-κB. - Wikidata - awgldk - TriplyDB

Ca2+/Calmodulin-dependent protein kinase II δ mediates myocardial ischemia/reperfusion injury through nuclear factor-κB.

Ca2+/Calmodulin-dependent protein kinase II δ mediates myocardial ischemia/reperfusion injury through nuclear factor-κB.

http://www.wikidata.org/entity/Q41584910

about

CaMKII oxidative activation and the pathogenesis of cardiac disease CaMKIIdelta subtypes: localization and function Protein methionine oxidation augments reperfusion injury in acute ischemic stroke CaMKII induces permeability transition through Drp1 phosphorylation during chronic β-AR stimulation Deletion of low molecular weight protein tyrosine phosphatase (Acp1) protects against stress-induced cardiomyopathy.CaMKII-dependent responses to ischemia and reperfusion challenges in the heart.Protein Kinase Signaling at the Crossroads of Myocyte Life and Death in Ischemic Heart Disease.MicroRNA-15a inhibition protects against hypoxia/reoxygenation-induced apoptosis of cardiomyocytes by targeting mothers against decapentaplegic homolog 7.NF-κB-modulated miR-130a targets TNF-α in cervical cancer cells Three ways to die suddenly: do they all require calcium calmodulin-dependent protein kinase II?In vivo selective expression of thyroid hormone receptor α1 in endothelial cells attenuates myocardial injury in experimental myocardial infarction in mice.CaMKII-dependent phosphorylation of cardiac ryanodine receptors regulates cell death in cardiac ischemia/reperfusion injury.Cardiac-specific suppression of NF-κB signaling prevents diabetic cardiomyopathy via inhibition of the renin-angiotensin system.CaM Kinase II mediates maladaptive post-infarct remodeling and pro-inflammatory chemoattractant signaling but not acute myocardial ischemia/reperfusion injury.Cardiomyocyte p65 nuclear factor-κB is necessary for compensatory adaptation to pressure overload Mitochondrial reprogramming induced by CaMKIIδ mediates hypertrophy decompensation Studies on the role of apoptosis after transient myocardial ischemia: genetic deletion of the executioner caspases-3 and -7 does not limit infarct size and ventricular remodeling.Loss of ATP-Sensitive Potassium Channel Surface Expression in Heart Failure Underlies Dysregulation of Action Potential Duration and Myocardial Vulnerability to Injury Nuclear Calcium/Calmodulin-dependent Protein Kinase II Signaling Enhances Cardiac Progenitor Cell Survival and Cardiac Lineage Commitment Activation of M3 cholinoceptors attenuates vascular injury after ischaemia/reperfusion by inhibiting the Ca2+/calmodulin-dependent protein kinase II pathway Reductions in the Cardiac Transient Outward K+ Current Ito Caused by Chronic β-Adrenergic Receptor Stimulation Are Partly Rescued by Inhibition of Nuclear Factor κB.Long non-coding RNA C2dat1 regulates CaMKIIδ expression to promote neuronal survival through the NF-κB signaling pathway following cerebral ischemia.Oxidant stress promotes disease by activating CaMKII.The promise of CaMKII inhibition for heart disease: preventing heart failure and arrhythmias.Myocyte signalling in leucocyte recruitment to the heart.Integrated mechanisms of CaMKII-dependent ventricular remodeling.The role of post-translational modifications in acute and chronic cardiovascular disease.Resuscitation of a dead cardiomyocyte.CaMKIIδ and cardiomyocyte Ca(2+) signalling new perspectives on splice variant targeting.Signaling Pathways in Cardiac Myocyte Apoptosis.Macrophage-epithelial interactions in pulmonary alveoli.CaMKII is a nodal signal for multiple programmed cell death pathways in heart.The role of miR-130a in cancer.Inducible cardiomyocyte-specific deletion of CaM kinase II protects from pressure overload-induced heart failure.CaMKIIδ subtypes differentially regulate infarct formation following ex vivo myocardial ischemia/reperfusion through NF-κB and TNF-α.Sex-dependent effects of chronic psychosocial stress on myocardial sensitivity to ischemic injury.NOD1, a new player in cardiac function and calcium handling.CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca(2+) leak and the pathophysiological response to chronic β-adrenergic stimulation.Smooth muscle CaMKIIδ promotes allergen-induced airway hyperresponsiveness and inflammation.CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress-induced myocardial necroptosis.

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Ca2+/Calmodulin-dependent protein kinase II δ mediates myocardial ischemia/reperfusion injury through nuclear factor-κB.

http://www.wikidata.org/entity/Q41584910

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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2013年论文

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2013年论文

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name

Ca2+/Calmodulin-dependent prot ...... ury through nuclear factor-κB.

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type

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Ca2+/Calmodulin-dependent prot ...... ury through nuclear factor-κB.

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Ca2+/Calmodulin-dependent prot ...... ury through nuclear factor-κB.

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CIRCRESAHA.112.276915

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Circulation Research

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Ca2+/Calmodulin-dependent prot ...... ury through nuclear factor-κB.

@en

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Alexander C Zambon

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

Charles B B Gray

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Haiyun Ling

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Joan Heller Brown

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Kirk Peterson

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Michael Grimm

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

Nancy Dalton

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Nicole H Purcell

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Yusu Gu

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P2860

Blockade of the natriuretic peptide receptor guanylyl cyclase-A inhibits NF-kappaB activation and alleviates myocardial ischemia/reperfusion injury

Identification of novel isoforms of the delta subunit of Ca2+/calmodulin-dependent protein kinase II. Differential expression in rat brain and aorta

Ventricular muscle-restricted targeting of the RXRalpha gene reveals a non-cell-autonomous requirement in cardiac chamber morphogenesis

A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation

Gene expression patterns define key transcriptional events in cell-cycle regulation by cAMP and protein kinase A.

Calcium/calmodulin-dependent protein kinase (CaMK) Ialpha mediates the macrophage inflammatory response to sepsis

CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo.

Role of the mitochondrial permeability transition in myocardial disease.

Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury

Inflammation, endoplasmic reticulum stress, autophagy, and the monocyte chemoattractant protein-1/CCR2 pathway.

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935-944

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10.1161/CIRCRESAHA.112.276915

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6

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112

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2013-02-06T00:00:00Z

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23388157

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reperfusion injury

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3673710

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