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

التفاصيل البيبلوغرافية
المؤلفون الرئيسيون:	Redwood, C, Robinson, P, Mirza, M, Knott, A, Marston, S, Watkins, H
التنسيق:	Conference item
منشور في:	2003

مواد مشابهة

HCM and DCM mutations in cardiac thin filament proteins have opposite effects on the regulation of contractility in vitro
حسب: Redwood, C, وآخرون
منشور في: (2003)

HCM and DCM mutations in thin filament proteins have opposite effects on in vitro motility
حسب: Marston, S, وآخرون
منشور في: (2002)

Effects of DCM mutations in thin filament regulatory proteins on contractile function
حسب: Robinson, P, وآخرون
منشور في: (2005)

In vitro motility studies of HCM and DCM mutations in cardiac muscle actin
حسب: Dyer, E, وآخرون
منشور في: (2007)

Mutations in tropomyosin that cause DCM, affect cooperativity of cardiac muscle thin filaments
حسب: Marston, S, وآخرون
منشور في: (2007)

Two DCM mutations in cardiac tropomyosin alter thin filament function by different mechanisms
حسب: Marston, S, وآخرون
منشور في: (2007)

Hypertrophic and dilated cardiomyopathycausing mutations of troponin and alpha-tropomyosin have opposite effects on thin filament calcium binding
حسب: Robinson, P, وآخرون
منشور في: (2007)

Autosomal dominant HCM and DCM phenotype caused by a novel mutation in phospholamban
حسب: Carballo, S, وآخرون
منشور في: (2004)

Two mutations in troponin I that cause hypertrophic cardiomyopathy have contrasting effects on cardiac muscle contractility.
حسب: Burton, D, وآخرون
منشور في: (2002)

Evidence for haploinsufficiency as the mechanism of action of MyBP-C mutations that cause HCM
حسب: Carballo, S, وآخرون
منشور في: (2008)

Dilated and hypertrophic cardiomyopathy mutations in troponin and alpha-tropomyosin have opposing effects on the calcium affinity of cardiac thin filaments.
حسب: Robinson, P, وآخرون
منشور في: (2007)

Dilated cardiomyopathy mutations in thin-filament regulatory proteins reduce contractility, suppress systolic Ca²⁺, and activate NFAT and Akt signaling
حسب: Robinson, P, وآخرون
منشور في: (2020)

Modulation of thin filament activation by breakdown or isoform switching of thin filament proteins: physiological and pathological implications.
حسب: Marston, S, وآخرون
منشور في: (2003)

Dilated cardiomyopathy mutations in three thin filament regulatory proteins result in a common functional phenotype.
حسب: Mirza, M, وآخرون
منشور في: (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.
حسب: Robinson, P, وآخرون
منشور في: (2002)

The effect of HCM mutations in troponin T and troponin I on the calcium binding of human cardiac troponin
حسب: Redwood, C, وآخرون
منشور في: (2001)

Functional effects of mutations in troponin T and tropomyosin which cause dilated cardiomyopathy
حسب: Robinson, P, وآخرون
منشور في: (2003)

MiR-1-3p that correlates with left ventricular function of HCM can serve as a potential target and differentiate HCM from DCM
حسب: Mengmeng Li, وآخرون
منشور في: (2018-06-01)

Mouse HCM Model Expression E99K ACTC Mutation Reproduces the Clinical HCM Phenotype
حسب: Song, W, وآخرون
منشور في: (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.
حسب: Mirza, M, وآخرون
منشور في: (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
حسب: Robinson, P, وآخرون
منشور في: (2007)

Mavacamten rescues increased myofilament calcium sensitivity and dysregulation of Ca2+ flux caused by thin filament hypertrophic cardiomyopathy mutations
حسب: Sparrow, AJ, وآخرون
منشور في: (2020)

A revised method of troponin exchange in permeabilised cardiac trabeculae using vanadate: functional consequences of a HCM-causing mutation in troponin I.
حسب: Preston, L, وآخرون
منشور في: (2006)

Interaction analyses elucidate the pathophysiology of HCM-causing missense mutations in cardiac myosin binding protein-C.
حسب: Moolman-Smook, J, وآخرون
منشور في: (2001)

Value of MRI derived parameters in the discrimination of familial left ventricular noncompaction (LVNC), DCM and HCM in comparison to healthy volunteers
حسب: Hassfeld Sabine, وآخرون
منشور في: (2011-02-01)

Functional investigation of troponin with the homozygous HCM mutation, TNNT2 K280N, obtained from an explanted heart
حسب: Bayliss, C, وآخرون
منشور في: (2012)

Familial Dilated Cardiomyopathy Caused by an Alpha-Tropomyosin Mutation: The Distinctive Natural History of Sarcomeric DCM
حسب: Lakdawala, N, وآخرون
منشور في: (2009)

Cardiomyopathy-Causing Mutations in Thin Filament Regulatory Proteins Acutely Affeect Ca2+-Buffering and Ca2+-Dependent Signalling In Situ
حسب: Robinson, P, وآخرون
منشور في: (2013)

P123The rescue of Ca2+ cycling abnormalities conferred by HCM-causing mutations with analogues of the green tea polyphenol epigallocatechin-3-gallate.
حسب: Robinson, P, وآخرون
منشور في: (2014)

The HCM-associated cardiac Troponin T mutation K280N causes reduced responsiveness to protein kinase A
حسب: Van Der Velden, J, وآخرون
منشور في: (2012)

Cardiomyopathy-causing mutations in cardiac thin filament regulatory proteins acutely affect Ca2+ buffering and Ca2+ dependant signalling in situ
حسب: Robinson, P, وآخرون
منشور في: (2012)

Comparison of the functional effects of mutations in troponin T which cause dilated and hypertrophic cardiomyopathies
حسب: Robinson, P, وآخرون
منشور في: (2002)

The nemaline myopathy-causing E117K mutation in β-tropomyosin reduces thin filament activation.
حسب: Karpicheva, O, وآخرون
منشور في: (2013)

Mutations in fast skeletal troponin I, troponin T and beta-tropomyosin that cause distal arthrogryposis all enhance thin filament activation
حسب: Robinson, P, وآخرون
منشور في: (2005)

A novel interaction between the C5 and C8 domains of myosin binding protein-C and its modulation by HCM mutations
حسب: Flashman, E, وآخرون
منشور في: (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.
حسب: Redwood, C, وآخرون
منشور في: (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.
حسب: Dass, S, وآخرون
منشور في: (2012)

Investigation of troponin I mutations causing familial hypertrophic cardiomyopathy
حسب: Abdulrazzak, H, وآخرون
منشور في: (2001)

Effects of hypertrophic cardiomyopathy mutations in troponin I on contractility of skinned cardiac muscle fibres
حسب: Burton, D, وآخرون
منشور في: (2002)

Functional effects of the DCM mutant Gly159Asp troponin C in skinned muscle fibres.
حسب: Preston, L, وآخرون
منشور في: (2007)