HCM and DCM mutations in thin filament proteins have opposite effects on regulation of contractility in vitro

HCM and DCM mutations in thin filament proteins have opposite effects on regulation of contractility in vitro

Bibliografische gegevens
Hoofdauteurs:	Redwood, C, Robinson, P, Mirza, M, Knott, A, Marston, S, Watkins, H
Formaat:	Conference item
Gepubliceerd in:	2003

Gelijkaardige items

HCM and DCM mutations in cardiac thin filament proteins have opposite effects on the regulation of contractility in vitro
door: Redwood, C, et al.
Gepubliceerd in: (2003)

HCM and DCM mutations in thin filament proteins have opposite effects on in vitro motility
door: Marston, S, et al.
Gepubliceerd in: (2002)

Effects of DCM mutations in thin filament regulatory proteins on contractile function
door: Robinson, P, et al.
Gepubliceerd in: (2005)

In vitro motility studies of HCM and DCM mutations in cardiac muscle actin
door: Dyer, E, et al.
Gepubliceerd in: (2007)

Mutations in tropomyosin that cause DCM, affect cooperativity of cardiac muscle thin filaments
door: Marston, S, et al.
Gepubliceerd in: (2007)

Two DCM mutations in cardiac tropomyosin alter thin filament function by different mechanisms
door: Marston, S, et al.
Gepubliceerd in: (2007)

Hypertrophic and dilated cardiomyopathycausing mutations of troponin and alpha-tropomyosin have opposite effects on thin filament calcium binding
door: Robinson, P, et al.
Gepubliceerd in: (2007)

Autosomal dominant HCM and DCM phenotype caused by a novel mutation in phospholamban
door: Carballo, S, et al.
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Two mutations in troponin I that cause hypertrophic cardiomyopathy have contrasting effects on cardiac muscle contractility.
door: Burton, D, et al.
Gepubliceerd in: (2002)

Evidence for haploinsufficiency as the mechanism of action of MyBP-C mutations that cause HCM
door: Carballo, S, et al.
Gepubliceerd in: (2008)

Dilated and hypertrophic cardiomyopathy mutations in troponin and alpha-tropomyosin have opposing effects on the calcium affinity of cardiac thin filaments.
door: Robinson, P, et al.
Gepubliceerd in: (2007)

Dilated cardiomyopathy mutations in thin-filament regulatory proteins reduce contractility, suppress systolic Ca²⁺, and activate NFAT and Akt signaling
door: Robinson, P, et al.
Gepubliceerd in: (2020)

Modulation of thin filament activation by breakdown or isoform switching of thin filament proteins: physiological and pathological implications.
door: Marston, S, et al.
Gepubliceerd in: (2003)

Dilated cardiomyopathy mutations in three thin filament regulatory proteins result in a common functional phenotype.
door: Mirza, M, et al.
Gepubliceerd in: (2005)

Alterations in thin filament regulation induced by a human cardiac troponin T mutant that causes dilated cardiomyopathy are distinct from those induced by troponin T mutants that cause hypertrophic cardiomyopathy.
door: Robinson, P, et al.
Gepubliceerd in: (2002)

The effect of HCM mutations in troponin T and troponin I on the calcium binding of human cardiac troponin
door: Redwood, C, et al.
Gepubliceerd in: (2001)

Functional effects of mutations in troponin T and tropomyosin which cause dilated cardiomyopathy
door: Robinson, P, et al.
Gepubliceerd in: (2003)

MiR-1-3p that correlates with left ventricular function of HCM can serve as a potential target and differentiate HCM from DCM
door: Mengmeng Li, et al.
Gepubliceerd in: (2018-06-01)

Mouse HCM Model Expression E99K ACTC Mutation Reproduces the Clinical HCM Phenotype
door: Song, W, et al.
Gepubliceerd in: (2009)

The effect of mutations in alpha-tropomyosin (E40K and E54K) that cause familial dilated cardiomyopathy on the regulatory mechanism of cardiac muscle thin filaments.
door: Mirza, M, et al.
Gepubliceerd in: (2007)

Using fluorescence emission spectroscopy to asses the Ca2+ affinity of reconstituted troponin and thin filaments containing cardiomyopathy causing mutations of troponin and alpha-tropomyosin
door: Robinson, P, et al.
Gepubliceerd in: (2007)

Mavacamten rescues increased myofilament calcium sensitivity and dysregulation of Ca2+ flux caused by thin filament hypertrophic cardiomyopathy mutations
door: Sparrow, AJ, et al.
Gepubliceerd in: (2020)

A revised method of troponin exchange in permeabilised cardiac trabeculae using vanadate: functional consequences of a HCM-causing mutation in troponin I.
door: Preston, L, et al.
Gepubliceerd in: (2006)

Interaction analyses elucidate the pathophysiology of HCM-causing missense mutations in cardiac myosin binding protein-C.
door: Moolman-Smook, J, et al.
Gepubliceerd in: (2001)

Value of MRI derived parameters in the discrimination of familial left ventricular noncompaction (LVNC), DCM and HCM in comparison to healthy volunteers
door: Hassfeld Sabine, et al.
Gepubliceerd in: (2011-02-01)

Functional investigation of troponin with the homozygous HCM mutation, TNNT2 K280N, obtained from an explanted heart
door: Bayliss, C, et al.
Gepubliceerd in: (2012)

Familial Dilated Cardiomyopathy Caused by an Alpha-Tropomyosin Mutation: The Distinctive Natural History of Sarcomeric DCM
door: Lakdawala, N, et al.
Gepubliceerd in: (2009)

Cardiomyopathy-Causing Mutations in Thin Filament Regulatory Proteins Acutely Affeect Ca2+-Buffering and Ca2+-Dependent Signalling In Situ
door: Robinson, P, et al.
Gepubliceerd in: (2013)

P123The rescue of Ca2+ cycling abnormalities conferred by HCM-causing mutations with analogues of the green tea polyphenol epigallocatechin-3-gallate.
door: Robinson, P, et al.
Gepubliceerd in: (2014)

The HCM-associated cardiac Troponin T mutation K280N causes reduced responsiveness to protein kinase A
door: Van Der Velden, J, et al.
Gepubliceerd in: (2012)

Cardiomyopathy-causing mutations in cardiac thin filament regulatory proteins acutely affect Ca2+ buffering and Ca2+ dependant signalling in situ
door: Robinson, P, et al.
Gepubliceerd in: (2012)

Comparison of the functional effects of mutations in troponin T which cause dilated and hypertrophic cardiomyopathies
door: Robinson, P, et al.
Gepubliceerd in: (2002)

The nemaline myopathy-causing E117K mutation in β-tropomyosin reduces thin filament activation.
door: Karpicheva, O, et al.
Gepubliceerd in: (2013)

Mutations in fast skeletal troponin I, troponin T and beta-tropomyosin that cause distal arthrogryposis all enhance thin filament activation
door: Robinson, P, et al.
Gepubliceerd in: (2005)

A novel interaction between the C5 and C8 domains of myosin binding protein-C and its modulation by HCM mutations
door: Flashman, E, et al.
Gepubliceerd in: (2002)

Investigation of a truncated cardiac troponin T that causes familial hypertrophic cardiomyopathy: Ca(2+) regulatory properties of reconstituted thin filaments depend on the ratio of mutant to wild-type protein.
door: Redwood, C, et al.
Gepubliceerd in: (2000)

Patients with hypertrophic cardiomyopathy (HCM) and HCM gene carriers have attenuated myocardial oxygenation response to vasodilator stress - a potential mechanism for sudden cardiac death.
door: Dass, S, et al.
Gepubliceerd in: (2012)

Investigation of troponin I mutations causing familial hypertrophic cardiomyopathy
door: Abdulrazzak, H, et al.
Gepubliceerd in: (2001)

Effects of hypertrophic cardiomyopathy mutations in troponin I on contractility of skinned cardiac muscle fibres
door: Burton, D, et al.
Gepubliceerd in: (2002)

Functional effects of the DCM mutant Gly159Asp troponin C in skinned muscle fibres.
door: Preston, L, et al.
Gepubliceerd in: (2007)