Myofibrillar Ca(2+) sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T. - Wikidata - awgldk - TriplyDB

Myofibrillar Ca(2+) sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T.

Myofibrillar Ca(2+) sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T.

http://www.wikidata.org/entity/Q54475335

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Why Is there a Limit to the Changes in Myofilament Ca2+-Sensitivity Associated with Myopathy Causing Mutations?Long 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 cardiomyopathy Familial dilated cardiomyopathy mutations uncouple troponin I phosphorylation from changes in myofibrillar Ca²⁺ sensitivity Investigations into the Sarcomeric Protein and Ca2+-Regulation Abnormalities Underlying Hypertrophic Cardiomyopathy in Cats (Felix catus).Investigating the role of uncoupling of troponin I phosphorylation from changes in myofibrillar Ca(2+)-sensitivity in the pathogenesis of cardiomyopathy.Computational modeling of Takotsubo cardiomyopathy: effect of spatially varying β-adrenergic stimulation in the rat left ventricle Z-band alternatively spliced PDZ motif protein (ZASP) is the major O-linked β-N-acetylglucosamine-substituted protein in human heart myofibrils The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin I OBSCN Mutations Associated with Dilated Cardiomyopathy and Haploinsufficiency.Best Practice BioBanking of Human Heart Tissue Uncoupling of myofilament Ca2+ sensitivity from troponin I phosphorylation by mutations can be reversed by epigallocatechin-3-gallate.Mutations in troponin T associated with Hypertrophic Cardiomyopathy increase Ca(2+)-sensitivity and suppress the modulation of Ca(2+)-sensitivity by troponin I phosphorylation.TPM3 deletions cause a hypercontractile congenital muscle stiffness phenotype.Contribution of Post-translational Phosphorylation to Sarcomere-Linked Cardiomyopathy Phenotypes.Irisin regulates cardiac physiology in zebrafish Pathogenesis associated with a restrictive cardiomyopathy mutant in cardiac troponin T is due to reduced protein stability and greatly increased myofilament Ca2+ sensitivity.Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes.Molecular Defects in Cardiac Myofilament Ca2+-Regulation Due to Cardiomyopathy-Linked Mutations Can Be Reversed by Small Molecules Binding to Troponin.

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Myofibrillar Ca(2+) sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T.

http://www.wikidata.org/entity/Q54475335

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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2012年學術文章

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name

Myofibrillar Ca

@nl

Myofibrillar Ca(2+) sensitivit ...... hy due to abnormal troponin T.

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type

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Myofibrillar Ca

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Myofibrillar Ca(2+) sensitivit ...... hy due to abnormal troponin T.

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Myofibrillar Ca

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Myofibrillar Ca(2+) sensitivit ...... hy due to abnormal troponin T.

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Cardiovascular Research

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Myofibrillar Ca(2+) sensitivit ...... hy due to abnormal troponin T.

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Adam M Jacques

http://www.w3.org/2001/XMLSchema#string

Andrew E Messer

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Charles S Redwood

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Christopher R Bayliss

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Clare E Gallon

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Cristobal Dos Remedios

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Man-Ching Leung

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O'Neal Copeland

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Steven B Marston

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P2860

Phosphorylation-dependent conformational transition of the cardiac specific N-extension of troponin I in cardiac troponin

Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations, and implications for a molecular diagnosis strategy

Cardiac myosin-binding protein C mutations and hypertrophic cardiomyopathy: haploinsufficiency, deranged phosphorylation, and cardiomyocyte dysfunction

Phosphorylation, but not alternative splicing or proteolytic degradation, is conserved in human and mouse cardiac troponin T

Troponin T isoform expression in humans. A comparison among normal and failing adult heart, fetal heart, and adult and fetal skeletal muscle

Evidence from human myectomy samples that MYBPC3 mutations cause hypertrophic cardiomyopathy through haploinsufficiency

The molecular phenotype of human cardiac myosin associated with hypertrophic obstructive cardiomyopathy

Analysis of cardiac myosin binding protein-C phosphorylation in human heart muscle

Thin filament mutations: developing an integrative approach to a complex disorder

The Genetic Basis for Cardiomyopathy

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500-508

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10.1093/CVR/CVS322

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3

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97

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William McKenna

Douglas G. Ward

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2012-10-24T00:00:00Z

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232700610

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23097574

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phosphorylation

hypertrophic obstructive cardiomyopathy