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

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

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

http://www.wikidata.org/entity/Q28267178

about

Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review Phosphorylation of protein kinase C sites Ser42/44 decreases Ca(2+)-sensitivity and blunts enhanced length-dependent activation in response to protein kinase A in human cardiomyocytes Protein kinase C alpha and epsilon phosphorylation of troponin and myosin binding protein C reduce Ca2+ sensitivity in human myocardium The C terminus of cardiac troponin I stabilizes the Ca2+-activated state of tropomyosin on actin filaments Why does troponin I have so many phosphorylation sites? Fact and fancy Cardiac thin filament regulation Length-dependent activation is modulated by cardiac troponin I bisphosphorylation at Ser23 and Ser24 but not by Thr143 phosphorylation A novel phosphorylation site, Serine 199, in the C-terminus of cardiac troponin I regulates calcium sensitivity and susceptibility to calpain-induced proteolysis TNNI1, TNNI2 and TNNI3: Evolution, regulation, and protein structure-function relationships.Combined troponin I Ser-150 and Ser-23/24 phosphorylation sustains thin filament Ca(2+) sensitivity and accelerates deactivation in an acidic environment.Computational studies of the effect of the S23D/S24D troponin I mutation on cardiac troponin structural dynamics.PKCα-specific phosphorylation of the troponin complex in human myocardium: a functional and proteomics analysis.Diastolic myofilament dysfunction in the failing human heart.Protein kinase A changes calcium sensitivity but not crossbridge kinetics in human cardiac myofibrils.Structural dynamics of C-domain of cardiac troponin I protein in reconstituted thin filament Engineered troponin C constructs correct disease-related cardiac myofilament calcium sensitivity.Effects of increased preload on the force-frequency response and contractile kinetics in early stages of cardiac muscle hypertrophy Regulation and physiological roles of the calpain system in muscular disorders Nitroxyl-mediated disulfide bond formation between cardiac myofilament cysteines enhances contractile function.Impact of site-specific phosphorylation of protein kinase A sites Ser23 and Ser24 of cardiac troponin I in human cardiomyocytes Cardiovascular proteomics: past, present, and future.Role of cardiac troponin I carboxy terminal mobile domain and linker sequence in regulating cardiac contraction.The functional significance of the last 5 residues of the C-terminus of cardiac troponin I.In vitro studies of early cardiac remodeling: impact on contraction and calcium handling.Ala scanning of the inhibitory region of cardiac troponin I.Synchronous in situ ATPase activity, mechanics, and Ca2+ sensitivity of human and porcine myocardium.New potential uses for cardiac troponins.Tri-modal regulation of cardiac muscle relaxation; intracellular calcium decline, thin filament deactivation, and cross-bridge cycling kinetics.Increased cross-bridge cycling kinetics after exchange of C-terminal truncated troponin I in skinned rat cardiac muscle.The Relaxation Properties of Myofibrils Are Compromised by Amino Acids that Stabilize α-Tropomyosin.Effect of troponin I Ser23/24 phosphorylation on Ca2+-sensitivity in human myocardium depends on the phosphorylation background.The Sydney Heart Bank: improving translational research while eliminating or reducing the use of animal models of human heart disease.Protein kinase C contributes to the maintenance of contractile force in human ventricular cardiomyocytes.Lys184 deletion in troponin I impairs relaxation kinetics and induces hypercontractility in murine cardiac myofibrils.Functional significance of C-terminal mobile domain of cardiac troponin I.Heart Failure-Related Hyperphosphorylation in the Cardiac Troponin I C Terminus Has Divergent Effects on Cardiac Function In Vivo.Proteomics analysis identified peroxiredoxin 2 involved in early-phase left ventricular impairment in hamsters with cardiomyopathy.

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P2860

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

http://www.wikidata.org/entity/Q28267178

description

2006 nî lūn-bûn

@nan

2006 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2006 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

Impaired diastolic function af ...... onin I in human cardiac muscle

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Impaired diastolic function af ...... onin I in human cardiac muscle

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Impaired diastolic function af ...... onin I in human cardiac muscle

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type

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Impaired diastolic function af ...... onin I in human cardiac muscle

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Impaired diastolic function af ...... onin I in human cardiac muscle

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Impaired diastolic function af ...... onin I in human cardiac muscle

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Impaired diastolic function af ...... onin I in human cardiac muscle

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Impaired diastolic function af ...... onin I in human cardiac muscle

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Impaired diastolic function af ...... onin I in human cardiac muscle

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Circulation Research

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Impaired diastolic function af ...... onin I in human cardiac muscle

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Alexandra Belus

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Anne M Murphy

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Beatrice Scellini

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Chiara Tesi

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Corrado Poggesi

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Cris dos Remedios

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Jennifer E van Eyk

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Kornelia Jaquet

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Nadiya A Narolska

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Nicky M Boontje

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1012-1020

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scholarly article

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10.1161/01.RES.0000248753.30340.AF

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Jolanda van der Velden

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2006-10-05T00:00:00Z

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17023673

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