Phosphorylation of troponin I by protein kinase A accelerates relaxation and crossbridge cycle kinetics in mouse ventricular muscle.
about
Cardiac troponin mutations and restrictive cardiomyopathyA troponin T mutation that causes infantile restrictive cardiomyopathy increases Ca2+ sensitivity of force development and impairs the inhibitory properties of troponinPhosphorylation of cardiac troponin I by mammalian sterile 20-like kinase 1TNNI3K is a novel mediator of myofilament function and phosphorylates cardiac troponin IMaturation status of sarcomere structure and function in human iPSC-derived cardiac myocytesPhosphorylation or glutamic acid substitution at protein kinase C sites on cardiac troponin I differentially depress myofilament tension and shortening velocityImpaired cardiac contractility response to hemodynamic stress in S100A1-deficient miceInhibition of PKC phosphorylation of cTnI improves cardiac performance in vivoLong term ablation of protein kinase A (PKA)-mediated cardiac troponin I phosphorylation leads to excitation-contraction uncoupling and diastolic dysfunction in a knock-in mouse model of hypertrophic cardiomyopathyThe heart-specific NH2-terminal extension regulates the molecular conformation and function of cardiac troponin IDistinct sarcomeric substrates are responsible for protein kinase D-mediated regulation of cardiac myofilament Ca2+ sensitivity and cross-bridge cyclingIn vivo left ventricular functional capacity is compromised in cMyBP-C null miceCaMKII induces permeability transition through Drp1 phosphorylation during chronic β-AR stimulationRemoval of the N-terminal extension of cardiac troponin I as a functional compensation for impaired myocardial beta-adrenergic signalingDifferential contribution of troponin I phosphorylation sites to the endothelin-modulated contractile responsePhospholemman is a negative feed-forward regulator of Ca2+ in β-adrenergic signaling, accelerating β-adrenergic inotropy.Removal of the cardiac troponin I N-terminal extension improves cardiac function in aged mice.Sexually dimorphic myofilament function and cardiac troponin I phosphospecies distribution in hypertrophic cardiomyopathy miceMolecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signalingRole of p90 ribosomal S6 kinase (p90RSK) in reactive oxygen species and protein kinase C beta (PKC-beta)-mediated cardiac troponin I phosphorylation.Protein Kinases as Drug Development Targets for Heart Disease TherapyCardiac troponin T, a sarcomeric AKAP, tethers protein kinase A at the myofilaments.Desensitization of myofilaments to Ca2+ as a therapeutic target for hypertrophic cardiomyopathy with mutations in thin filament proteins.Phosphorylation of cardiac troponin I at protein kinase C site threonine 144 depresses cooperative activation of thin filaments.Calcium sensitivity, force frequency relationship and cardiac troponin I: critical role of PKA and PKC phosphorylation sitesWhat we know and do not know about sex and cardiac disease.Regulation of contraction in mammalian striated muscles--the plot thick-ens.Ryanodine receptors: structure, expression, molecular details, and function in calcium release.Investigating the role of uncoupling of troponin I phosphorylation from changes in myofibrillar Ca(2+)-sensitivity in the pathogenesis of cardiomyopathy.PKA phosphorylation of cardiac troponin I modulates activation and relaxation kinetics of ventricular myofibrils.Force kinetics and individual sarcomere dynamics in cardiac myofibrils after rapid ca(2+) changes.Computational studies of the effect of the S23D/S24D troponin I mutation on cardiac troponin structural dynamics.Protein kinase A-induced myofilament desensitization to Ca(2+) as a result of phosphorylation of cardiac myosin-binding protein CMore severe cellular phenotype in human idiopathic dilated cardiomyopathy compared to ischemic heart disease.Novel function of cardiac protein kinase D1 as a dynamic regulator of Ca2+ sensitivity of contractionFibronectin increases the force production of mouse papillary muscles via α5β1 integrinIschemia reperfusion dysfunction changes model-estimated kinetics of myofilament interaction due to inotropic drugs in isolated hearts.The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin IMyofilament calcium sensitization delays decompensated hypertrophy differently between the sexes following myocardial infarctionProtein phosphorylation and signal transduction in cardiac thin filaments.
P2860
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P2860
Phosphorylation of troponin I by protein kinase A accelerates relaxation and crossbridge cycle kinetics in mouse ventricular muscle.
description
2001 nî lūn-bûn
@nan
2001年の論文
@ja
2001年学术文章
@wuu
2001年学术文章
@zh
2001年学术文章
@zh-cn
2001年学术文章
@zh-hans
2001年学术文章
@zh-my
2001年学术文章
@zh-sg
2001年學術文章
@yue
2001年學術文章
@zh-hant
name
Phosphorylation of troponin I ...... s in mouse ventricular muscle.
@en
Phosphorylation of troponin I ...... s in mouse ventricular muscle.
@nl
type
label
Phosphorylation of troponin I ...... s in mouse ventricular muscle.
@en
Phosphorylation of troponin I ...... s in mouse ventricular muscle.
@nl
prefLabel
Phosphorylation of troponin I ...... s in mouse ventricular muscle.
@en
Phosphorylation of troponin I ...... s in mouse ventricular muscle.
@nl
P2093
P356
P1433
P1476
Phosphorylation of troponin I ...... s in mouse ventricular muscle.
@en
P2093
Kentish JC
McCloskey DT
P304
P356
10.1161/HH1001.091640
P577
2001-05-01T00:00:00Z