Functional consequences of caspase activation in cardiac myocytes - Test2 - elhamkhani - TriplyDB

Functional consequences of caspase activation in cardiac myocytes

Functional consequences of caspase activation in cardiac myocytes

http://www.wikidata.org/entity/Q28215640

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Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review The subunit CSN6 of the COP9 signalosome is cleaved during apoptosis Essential myosin light chain as a target for caspase-3 in failing myocardium Intrinsic-mediated caspase activation is essential for cardiomyocyte hypertrophy Pathophysiology of sepsis-induced myocardial dysfunction Identification of a functionally critical protein kinase C phosphorylation residue of cardiac troponin T Selective deletion of the NH2-terminal variable region of cardiac troponin T in ischemia reperfusion by myofibril-associated mu-calpain cleavage Pathogenic properties of the N-terminal region of cardiac myosin binding protein-C in vitro Restricted N-terminal truncation of cardiac troponin T: a novel mechanism for functional adaptation to energetic crisis Troponin T core structure and the regulatory NH2-terminal variable region Troponin T isoforms and posttranscriptional modifications: Evolution, regulation and function Cardiomyocyte apoptosis triggered by RAFTK/pyk2 via Src kinase is antagonized by paxillin Troponin T modulates sarcomere length-dependent recruitment of cross-bridges in cardiac muscle.PYRROLO[1,2-b][1,2,5]BENZOTHIADIAZEPINES (PBTDs) induce apoptosis in K562 cells.Induction of apoptosis by d-limonene is mediated by a caspase-dependent mitochondrial death pathway in human leukemia cells.Obesity and preclinical changes of cardiac geometry and function.Hyperglycemia-induced diaphragm weakness is mediated by oxidative stress.Caspase-3 knock-down reverses contractile dysfunction induced by sepsis in adult rat ventricular myocytes Caspase inhibition modulates left ventricular remodeling following myocardial infarction through cellular and extracellular mechanisms.Apoptosis by [Pt(O,O'-acac)(γ-acac)(DMS)] requires PKC-δ mediated p53 activation in malignant pleural mesothelioma.Cardiac remodeling in obesity.Hydrogen sulfide attenuates cardiac dysfunction in a rat model of heart failure: a mechanism through cardiac mitochondrial protection Top-down mass spectrometry of cardiac myofilament proteins in health and disease.TNF-α-induced cardiomyocyte apoptosis contributes to cardiac dysfunction after coronary microembolization in mini-pigs The role of the Hsp90/Akt pathway in myocardial calpain-induced caspase-3 activation and apoptosis during sepsis.Grape seed proanthocyanidins induce apoptosis through p53, Bax, and caspase 3 pathways.A mechanistic role for cardiac myocyte apoptosis in heart failure.Rare incidence of congestive heart failure in gastrointestinal stromal tumor and other sarcoma patients receiving imatinib mesylate.The influence of lung ischemia-reperfusion injury on myocardium Targeting ischemic cardiac dysfunction through gene transfer.Elevated levels of uterine anti-apoptotic signaling may activate NFKB and potentially confer resistance to caspase 3-mediated apoptotic cell death during pregnancy in mice.Circulating levels of cytochrome c after resuscitation from cardiac arrest: a marker of mitochondrial injury and predictor of survival.Antiapoptotic signaling via MCL1 confers resistance to caspase-3-mediated apoptotic cell death in the pregnant human uterine myocyte.Inhibition of caspase mediated apoptosis restores muscle function after crush injury in rat skeletal muscle Prevention of postoperative atrial fibrillation: novel and safe strategy based on the modulation of the antioxidant system TNF provokes cardiomyocyte apoptosis and cardiac remodeling through activation of multiple cell death pathways The N-terminal extension of cardiac troponin T stabilizes the blocked state of cardiac thin filament Don't lose heart--therapeutic value of apoptosis prevention in the treatment of cardiovascular disease.Heart failure, myocardial stunning, and troponin: a key regulator of the cardiac myofilament.Significance and interpretation of elevated troponin in septic patients

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P2860

Functional consequences of caspase activation in cardiac myocytes

http://www.wikidata.org/entity/Q28215640

description

2002 nî lūn-bûn

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2002 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2002 թվականի ապրիլին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

Functional consequences of caspase activation in cardiac myocytes

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Functional consequences of caspase activation in cardiac myocytes

@en

Functional consequences of caspase activation in cardiac myocytes

@nl

type

label

Functional consequences of caspase activation in cardiac myocytes

@ast

Functional consequences of caspase activation in cardiac myocytes

@en

Functional consequences of caspase activation in cardiac myocytes

@nl

prefLabel

Functional consequences of caspase activation in cardiac myocytes

@ast

Functional consequences of caspase activation in cardiac myocytes

@en

Functional consequences of caspase activation in cardiac myocytes

@nl

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Functional consequences of caspase activation in cardiac myocytes

@en

P2093

Catherine Communal

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

Marius Sumandea

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

Pieter de Tombe

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

R John Solaro

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

Roger J Hajjar

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P2860

Significance of myocytes with positive DNA in situ nick end-labeling (TUNEL) in hearts with dilated cardiomyopathy: not apoptosis but DNA repair.

The role of the cytoskeleton in heart failure.

Myofilament calcium regulation in human myocardium

Manipulating the contractile apparatus: genetically defined animal models of cardiovascular disease.

Apoptosis in heart failure: release of cytochrome c from mitochondria and activation of caspase-3 in human cardiomyopathy.

Protein kinase A does not alter economy of force maintenance in skinned rat cardiac trabeculae.

Molecular genetic studies of familial hypertrophic cardiomyopathy.

Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the beta-adrenergic pathway.

Increased expression of isoform 1 of the sarcoplasmic reticulum Ca(2+)-release channel in failing human heart.

Inhibition of caspase-3 improves contractile recovery of stunned myocardium, independent of apoptosis-inhibitory effects.

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10.1073/PNAS.092022999

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9

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99

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11396464

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11972044

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122935

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