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

מידע ביבליוגרפי
Main Authors:	Redwood, C, Robinson, P, Mirza, M, Knott, A, Marston, S, Watkins, H
פורמט:	Conference item
יצא לאור:	2003

פריטים דומים

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Investigation of troponin I mutations causing familial hypertrophic cardiomyopathy
מאת: Abdulrazzak, H, et al.
יצא לאור: (2001)

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

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