Lys184 deletion in troponin I impairs relaxation kinetics and induces hypercontractility in murine cardiac myofibrils. - Wikidata - awgldk - TriplyDB

Lys184 deletion in troponin I impairs relaxation kinetics and induces hypercontractility in murine cardiac myofibrils.

Lys184 deletion in troponin I impairs relaxation kinetics and induces hypercontractility in murine cardiac myofibrils.

http://www.wikidata.org/entity/Q46445601

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Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review TNNI1, TNNI2 and TNNI3: Evolution, regulation, and protein structure-function relationships.Pathogenic peptide deviations support a model of adaptive evolution of chordate cardiac performance by troponin mutations.Epigallocatechin-3-Gallate Accelerates Relaxation and Ca2+ Transient Decay and Desensitizes Myofilaments in Healthy and Mybpc3-Targeted Knock-in Cardiomyopathic Mice.The curious role of sarcomeric proteins in control of diverse processes in cardiac myocytes.Deletion of the titin N2B region accelerates myofibrillar force development but does not alter relaxation kinetics Disease-related cardiac troponins alter thin filament Ca2+ association and dissociation rates.Strong cross-bridges potentiate the Ca(2+) affinity changes produced by hypertrophic cardiomyopathy cardiac troponin C mutants in myofilaments: a fast kinetic approach.The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin I Micromechanical function of myofibrils isolated from skeletal and cardiac muscles of the zebrafish.Engineered troponin C constructs correct disease-related cardiac myofilament calcium sensitivity.Instrumentation to study myofibril mechanics from static to artificial simulations of cardiac cycle.Mechanical and energetic properties of papillary muscle from ACTC E99K transgenic mouse models of hypertrophic cardiomyopathy.Postnatal Development of Right Ventricular Myofibrillar Biomechanics in Relation to the Sarcomeric Protein Phenotype in Pediatric Patients with Conotruncal Heart Defects The Zebrafish Heart as a Model of Mammalian Cardiac Function.Arginylation regulates myofibrils to maintain heart function and prevent dilated cardiomyopathy.Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effects in vivo in a mouse model of hypertrophic cardiomyopathy.Emerging pharmacologic and structural therapies for hypertrophic cardiomyopathy.

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Lys184 deletion in troponin I impairs relaxation kinetics and induces hypercontractility in murine cardiac myofibrils.

http://www.wikidata.org/entity/Q46445601

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年學術文章

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name

Lys184 deletion in troponin I ...... in murine cardiac myofibrils.

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Lys184 deletion in troponin I ...... in murine cardiac myofibrils.

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type

label

Lys184 deletion in troponin I ...... in murine cardiac myofibrils.

@en

Lys184 deletion in troponin I ...... in murine cardiac myofibrils.

@nl

prefLabel

Lys184 deletion in troponin I ...... in murine cardiac myofibrils.

@en

Lys184 deletion in troponin I ...... in murine cardiac myofibrils.

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Cardiovascular Research

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Lys184 deletion in troponin I ...... y in murine cardiac myofibrils

@en

P2093

Alfredo J Lopez Davila

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Bogdan Iorga

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Gabriele Pfitzer

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Ina Stehle

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Johannes Solzin

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Natascha Blaudeck

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Robert Stehle

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P2860

Functional consequences of the mutations in human cardiac troponin I gene found in familial hypertrophic cardiomyopathy

Impaired diastolic function after exchange of endogenous troponin I with C-terminal truncated troponin I in human cardiac muscle

Effect of Ca2+ on cross-bridge turnover kinetics in skinned single rabbit psoas fibers: implications for regulation of muscle contraction.

Hypertrophic cardiomyopathy: a systematic review.

Force kinetics and individual sarcomere dynamics in cardiac myofibrils after rapid ca(2+) changes.

Ising model of cardiac thin filament activation with nearest-neighbor cooperative interactions

Cellular and molecular aspects of familial hypertrophic cardiomyopathy caused by mutations in the cardiac troponin I gene.

Sarcomeric determinants of striated muscle relaxation kinetics.

Kinetic mechanism of the Ca2+-dependent switch-on and switch-off of cardiac troponin in myofibrils.

Myofilament-generated tension oscillations during partial calcium activation and activation dependence of the sarcomere length-tension relation of skinned cardiac cells.

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676-686

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10.1093/CVR/CVM113

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4

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77

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2007-12-20T00:00:00Z

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5751694

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18096573

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