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

Bibliográfalaš dieđut
Váldodahkkit:	Redwood, C, Robinson, P, Mirza, M, Knott, A, Marston, S, Watkins, H
Materiálatiipa:	Conference item
Almmustuhtton:	2003

Geahča maid

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

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

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

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

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

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

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

Autosomal dominant HCM and DCM phenotype caused by a novel mutation in phospholamban
Dahkki: Carballo, S, et al.
Almmustuhtton: (2004)

Two mutations in troponin I that cause hypertrophic cardiomyopathy have contrasting effects on cardiac muscle contractility.
Dahkki: Burton, D, et al.
Almmustuhtton: (2002)

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

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

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

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

Dilated cardiomyopathy mutations in three thin filament regulatory proteins result in a common functional phenotype.
Dahkki: Mirza, M, et al.
Almmustuhtton: (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.
Dahkki: Robinson, P, et al.
Almmustuhtton: (2002)

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

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

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

Mouse HCM Model Expression E99K ACTC Mutation Reproduces the Clinical HCM Phenotype
Dahkki: Song, W, et al.
Almmustuhtton: (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.
Dahkki: Mirza, M, et al.
Almmustuhtton: (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
Dahkki: Robinson, P, et al.
Almmustuhtton: (2007)

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

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

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

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

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

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

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

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

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

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

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

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

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

A novel interaction between the C5 and C8 domains of myosin binding protein-C and its modulation by HCM mutations
Dahkki: Flashman, E, et al.
Almmustuhtton: (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.
Dahkki: Redwood, C, et al.
Almmustuhtton: (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.
Dahkki: Dass, S, et al.
Almmustuhtton: (2012)

Investigation of troponin I mutations causing familial hypertrophic cardiomyopathy
Dahkki: Abdulrazzak, H, et al.
Almmustuhtton: (2001)

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

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