Increased myofilament Ca2+ sensitivity and diastolic dysfunction as early consequences of Mybpc3 mutation in heterozygous knock-in mice
about
Animal and in silico models for the study of sarcomeric cardiomyopathiesTargets for therapy in sarcomeric cardiomyopathiesResearch priorities in sarcomeric cardiomyopathiesWhy Is there a Limit to the Changes in Myofilament Ca2+-Sensitivity Associated with Myopathy Causing Mutations?Diastolic dysfunctionEndothelin-1 induces myofibrillar disarray and contractile vector variability in hypertrophic cardiomyopathy-induced pluripotent stem cell-derived cardiomyocytesModelling sarcomeric cardiomyopathies in the dish: from human heart samples to iPSC cardiomyocytesTetrahydrobiopterin improves diastolic dysfunction by reversing changes in myofilament propertiesPerturbed length-dependent activation in human hypertrophic cardiomyopathy with missense sarcomeric gene mutationsRescue of cardiomyopathy through U7snRNA-mediated exon skipping in Mybpc3-targeted knock-in miceRepair of Mybpc3 mRNA by 5'-trans-splicing in a Mouse Model of Hypertrophic CardiomyopathyEpigallocatechin-3-Gallate Accelerates Relaxation and Ca2+ Transient Decay and Desensitizes Myofilaments in Healthy and Mybpc3-Targeted Knock-in Cardiomyopathic Mice.Impact of ANKRD1 mutations associated with hypertrophic cardiomyopathy on contraction parameters of engineered heart tissue.FHL2 expression and variants in hypertrophic cardiomyopathy.Cardiac troponin I Pro82Ser variant induces diastolic dysfunction, blunts β-adrenergic response, and impairs myofilament cooperativityHaploinsufficiency of MYBPC3 exacerbates the development of hypertrophic cardiomyopathy in heterozygous mice.Molecular Screen Identifies Cardiac Myosin-Binding Protein-C as a Protein Kinase G-Iα Substrate.Mechanical and energetic properties of papillary muscle from ACTC E99K transgenic mouse models of hypertrophic cardiomyopathy.Impaired contractile function due to decreased cardiac myosin binding protein C content in the sarcomereE258K HCM-causing mutation in cardiac MyBP-C reduces contractile force and accelerates twitch kinetics by disrupting the cMyBP-C and myosin S2 interaction.Contractile dysfunction in a mouse model expressing a heterozygous MYBPC3 mutation associated with hypertrophic cardiomyopathy.Myocardial energetics in heart failure.Cardiac myosin-binding protein-C is a critical mediator of diastolic function.I-1-deficiency negatively impacts survival in a cardiomyopathy mouse model.Cellular and Molecular Aspects of Dyssynchrony and Resynchronization.Contractile Defect Caused by Mutation in MYBPC3 Revealed under Conditions Optimized for Human PSC-Cardiomyocyte FunctionLoss of myocardial retinoic acid receptor α induces diastolic dysfunction by promoting intracellular oxidative stress and calcium mishandling in adult mice.Selective phosphorylation of PKA targets after β-adrenergic receptor stimulation impairs myofilament function in Mybpc3-targeted HCM mouse model.Genetically Encoded Biosensors Reveal PKA Hyperphosphorylation on the Myofilaments in Rabbit Heart Failure.Nebivolol Desensitizes Myofilaments of a Hypertrophic Cardiomyopathy Mouse Model.Deficient cMyBP-C protein expression during cardiomyocyte differentiation underlies human hypertrophic cardiomyopathy cellular phenotypes in disease specific human ES cell derived cardiomyocytes.Diltiazem prevents stress-induced contractile deficits in cardiomyocytes, but does not reverse the cardiomyopathy phenotype in Mybpc3-knock-in mice.Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy.Effects of long-term atorvastatin treatment on cardiac aging.Clinical outcomes associated with sarcomere mutations in hypertrophic cardiomyopathy: a meta-analysis on 7675 individuals.IGF-IR signaling attenuates the age-related decline of diastolic cardiac function.Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effects in vivo in a mouse model of hypertrophic cardiomyopathy.Echocardiographic evaluation of diastolic function in mouse models of heart disease.Sexual dimorphic response to exercise in hypertrophic cardiomyopathy-associated MYBPC3-targeted knock-in mice.Genotype-Dependent and -Independent Calcium Signaling Dysregulation in Human Hypertrophic Cardiomyopathy.
P2860
Q26865437-8C1E2A2D-E76B-4803-A953-D4E296F8A850Q27027023-8AFD1B16-40FE-40E8-A60E-F6C872897166Q27694507-B93EE8D9-BB2B-4155-95A5-333EF4E9762AQ28079573-6D3B5C8E-88E2-4F08-BF04-05A55C592A72Q28087715-84A95AC1-EAE5-4B2C-9C01-38FA0476F52BQ28251448-12629F47-E2F4-41D5-9F6D-1207DA0D4233Q28255887-856F9AAB-DBC0-4102-8DF6-3A580CE1317EQ28281608-103AA442-2C7E-4431-A9C8-CB4EA057A821Q28287468-C7F5D60E-4979-4082-8B52-6DB9728744FCQ28291547-52454051-BE79-426D-BB6B-480E53D63A11Q28293833-42CBF6F6-3AA6-4367-9E37-506A649F86BBQ30830714-65FB09A5-7B1A-4687-AA51-626DB966A2D3Q34338236-A3D44AA2-4132-41C4-85DF-6DBCFC737A3DQ34430364-4FEC2FB8-C705-4824-B149-AC52DCD5CC86Q34980505-089DD997-7E40-4A8B-8FCC-A0A2FF463D9DQ36272676-1134DFE8-3107-4BE5-AE3C-2FE572C88628Q36296869-29FA0DE9-8B40-4346-859F-1958C61FF552Q36923785-C740CD6B-D40F-4C4D-90DE-D63CABB442D0Q37054964-D9CFD90A-EA80-41D4-86D0-E1EC9A83E018Q37121972-8864F8EE-4943-436B-A046-58C8A9AEAD1DQ37629210-F39EDF77-46E8-4BCD-B72C-209EF5243F11Q38112349-0B8DADE7-572A-48A2-BF38-A72113B8E9BEQ38179957-D8311427-21AC-48C5-9F13-DC5829542C8CQ38635697-63791F6F-AB36-4DA4-B6C7-9EBD4AF09AC2Q38644094-F2CFD985-5EC8-4E14-A662-1411F249D7A4Q38826141-64712F16-26A7-41BC-A94E-9D0B9A882155Q39475312-773C3130-A8BA-41DF-BF39-78EE3B4D7B38Q40042653-8D4E36E1-3631-4A95-8E78-81298D25A309Q40601692-2EF1EC9D-627A-4BEE-B2B9-108D443B0D20Q41203153-4F175066-5D54-44A4-B3F5-B2B471208ED4Q41700317-B3C06129-D43C-45DF-8A84-4E611F02053EQ42504304-C001575F-E47A-4EDD-969B-3F234346F915Q42515078-3D093712-EF9A-423E-9922-A6D672C2EE7EQ42962896-3B371014-284C-4757-B189-419530D0A347Q48177445-1AFAD7A2-FE86-42E3-85B8-615602130428Q48681237-A0CDD858-6220-4660-8596-2A5B943EF668Q48747768-61086CD6-EF91-449F-A4F9-13D8F346B868Q49345522-0CEE929A-2313-4F60-91C2-81BB12B0BF5DQ51128798-F68D6146-1ADA-4EEF-BF18-73D8F69BB36AQ51446174-1BA75128-16D7-4882-BE4D-EA33E065B241
P2860
Increased myofilament Ca2+ sensitivity and diastolic dysfunction as early consequences of Mybpc3 mutation in heterozygous knock-in mice
description
2012 nî lūn-bûn
@nan
2012 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
name
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@ast
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@en
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@nl
type
label
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@ast
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@en
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@nl
prefLabel
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@ast
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@en
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@nl
P2093
P2860
P50
P3181
P1476
Increased myofilament Ca2+ sen ...... in heterozygous knock-in mice
@en
P2093
Bodvaël Fraysse
Catherine Coirault
Florian Weinberger
Friederike Cuello
Jonathan C Kentish
Jutta Starbatty
Nicolas Vignier
Sonya C Bardswell
Thomas Eschenhagen
P2860
P304
P3181
P356
10.1016/J.YJMCC.2012.03.009
P407
P577
2012-06-01T00:00:00Z