Calcium sensitivity and the Frank-Starling mechanism of the heart are increased in titin N2B region-deficient mice
about
Maturing human pluripotent stem cell-derived cardiomyocytes in human engineered cardiac tissuesAutomated analysis of contractile force and Ca2+ transients in engineered heart tissue.Integrating multi-scale data to create a virtual physiological mouse heart.Deletion of the titin N2B region accelerates myofibrillar force development but does not alter relaxation kineticsContribution of titin and extracellular matrix to passive pressure and measurement of sarcomere length in the mouse left ventricle.Thick-filament strain and interfilament spacing in passive muscle: effect of titin-based passive tensionThe giant protein titin: a regulatory node that integrates myocyte signaling pathways.Myosin head orientation: a structural determinant for the Frank-Starling relationshipMechanics on myocardium deficient in the N2B region of titin: the cardiac-unique spring element improves efficiency of the cardiac cycle.Magnitude of length-dependent changes in contractile properties varies with titin isoform in rat ventricles.Stretch of contracting cardiac muscle abruptly decreases the rate of phosphate release at high and low calcium.Phosphorylating Titin's Cardiac N2B Element by ERK2 or CaMKIIδ Lowers the Single Molecule and Cardiac Muscle ForceCardiac Myosin Binding Protein-C Phosphorylation Modulates Myofilament Length-Dependent ActivationCalcium sensitivity and myofilament lattice structure in titin N2B KO mice.CaMKII effects on inotropic but not lusitropic force frequency responses require phospholamban.Impact of myocyte strain on cardiac myofilament activationCardiac tissue structure, properties, and performance: a materials science perspective.The genetic landscape of cardiomyopathy and its role in heart failure.Tampering with springs: phosphorylation of titin affecting the mechanical function of cardiomyocytes.Distinct contributions of the thin and thick filaments to length-dependent activation in heart muscle.Reducing RBM20 activity improves diastolic dysfunction and cardiac atrophy.Preserved cross-bridge kinetics in human hypertrophic cardiomyopathy patients with MYBPC3 mutations.An analysis of deformation-dependent electromechanical coupling in the mouse heart.Organ-level right ventricular dysfunction with preserved Frank-Starling mechanism in a mouse model of pulmonary arterial hypertension.
P2860
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P2860
Calcium sensitivity and the Frank-Starling mechanism of the heart are increased in titin N2B region-deficient mice
description
2010 nî lūn-bûn
@nan
2010 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@ast
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@en
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@nl
type
label
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@ast
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@en
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@nl
prefLabel
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@ast
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@en
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@nl
P2093
P2860
P1476
Calcium sensitivity and the Fr ...... itin N2B region-deficient mice
@en
P2093
Eun-Jeong Lee
Henk L Granzier
P2860
P304
P356
10.1016/J.YJMCC.2010.05.006
P577
2010-05-23T00:00:00Z