Lys184 deletion in troponin I impairs relaxation kinetics and induces hypercontractility in murine cardiac myofibrils.
about
Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused reviewTNNI1, 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 kineticsDisease-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 IMicromechanical 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 DefectsThe 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.
P2860
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P2860
Lys184 deletion in troponin I impairs relaxation kinetics and induces hypercontractility in murine cardiac myofibrils.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
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2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
2007年學術文章
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2007年學術文章
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name
Lys184 deletion in troponin I ...... in murine cardiac myofibrils.
@en
Lys184 deletion in troponin I ...... in murine cardiac myofibrils.
@nl
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.
@nl
P2093
P2860
P356
P1476
Lys184 deletion in troponin I ...... y in murine cardiac myofibrils
@en
P2093
Alfredo J Lopez Davila
Bogdan Iorga
Gabriele Pfitzer
Ina Stehle
Johannes Solzin
Natascha Blaudeck
Robert Stehle
P2860
P304
P356
10.1093/CVR/CVM113
P50
P577
2007-12-20T00:00:00Z