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

Detaylı Bibliyografya
Asıl Yazarlar:	Redwood, C, Robinson, P, Mirza, M, Knott, A, Marston, S, Watkins, H
Materyal Türü:	Conference item
Baskı/Yayın Bilgisi:	2003

HCM and DCM mutations in cardiac thin filament proteins have opposite effects on the regulation of contractility in vitro
Yazar:: Redwood, C, ve diğerleri
Baskı/Yayın Bilgisi: (2003)

HCM and DCM mutations in thin filament proteins have opposite effects on in vitro motility
Yazar:: Marston, S, ve diğerleri
Baskı/Yayın Bilgisi: (2002)

Effects of DCM mutations in thin filament regulatory proteins on contractile function
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2005)

In vitro motility studies of HCM and DCM mutations in cardiac muscle actin
Yazar:: Dyer, E, ve diğerleri
Baskı/Yayın Bilgisi: (2007)

Mutations in tropomyosin that cause DCM, affect cooperativity of cardiac muscle thin filaments
Yazar:: Marston, S, ve diğerleri
Baskı/Yayın Bilgisi: (2007)

Two DCM mutations in cardiac tropomyosin alter thin filament function by different mechanisms
Yazar:: Marston, S, ve diğerleri
Baskı/Yayın Bilgisi: (2007)

Hypertrophic and dilated cardiomyopathycausing mutations of troponin and alpha-tropomyosin have opposite effects on thin filament calcium binding
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2007)

Autosomal dominant HCM and DCM phenotype caused by a novel mutation in phospholamban
Yazar:: Carballo, S, ve diğerleri
Baskı/Yayın Bilgisi: (2004)

Two mutations in troponin I that cause hypertrophic cardiomyopathy have contrasting effects on cardiac muscle contractility.
Yazar:: Burton, D, ve diğerleri
Baskı/Yayın Bilgisi: (2002)

Evidence for haploinsufficiency as the mechanism of action of MyBP-C mutations that cause HCM
Yazar:: Carballo, S, ve diğerleri
Baskı/Yayın Bilgisi: (2008)

Dilated and hypertrophic cardiomyopathy mutations in troponin and alpha-tropomyosin have opposing effects on the calcium affinity of cardiac thin filaments.
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2007)

Dilated cardiomyopathy mutations in thin-filament regulatory proteins reduce contractility, suppress systolic Ca²⁺, and activate NFAT and Akt signaling
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2020)

Modulation of thin filament activation by breakdown or isoform switching of thin filament proteins: physiological and pathological implications.
Yazar:: Marston, S, ve diğerleri
Baskı/Yayın Bilgisi: (2003)

Dilated cardiomyopathy mutations in three thin filament regulatory proteins result in a common functional phenotype.
Yazar:: Mirza, M, ve diğerleri
Baskı/Yayın Bilgisi: (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.
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2002)

The effect of HCM mutations in troponin T and troponin I on the calcium binding of human cardiac troponin
Yazar:: Redwood, C, ve diğerleri
Baskı/Yayın Bilgisi: (2001)

Functional effects of mutations in troponin T and tropomyosin which cause dilated cardiomyopathy
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2003)

MiR-1-3p that correlates with left ventricular function of HCM can serve as a potential target and differentiate HCM from DCM
Yazar:: Mengmeng Li, ve diğerleri
Baskı/Yayın Bilgisi: (2018-06-01)

Mouse HCM Model Expression E99K ACTC Mutation Reproduces the Clinical HCM Phenotype
Yazar:: Song, W, ve diğerleri
Baskı/Yayın Bilgisi: (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.
Yazar:: Mirza, M, ve diğerleri
Baskı/Yayın Bilgisi: (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
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2007)

Mavacamten rescues increased myofilament calcium sensitivity and dysregulation of Ca2+ flux caused by thin filament hypertrophic cardiomyopathy mutations
Yazar:: Sparrow, AJ, ve diğerleri
Baskı/Yayın Bilgisi: (2020)

A revised method of troponin exchange in permeabilised cardiac trabeculae using vanadate: functional consequences of a HCM-causing mutation in troponin I.
Yazar:: Preston, L, ve diğerleri
Baskı/Yayın Bilgisi: (2006)

Interaction analyses elucidate the pathophysiology of HCM-causing missense mutations in cardiac myosin binding protein-C.
Yazar:: Moolman-Smook, J, ve diğerleri
Baskı/Yayın Bilgisi: (2001)

Value of MRI derived parameters in the discrimination of familial left ventricular noncompaction (LVNC), DCM and HCM in comparison to healthy volunteers
Yazar:: Hassfeld Sabine, ve diğerleri
Baskı/Yayın Bilgisi: (2011-02-01)

Functional investigation of troponin with the homozygous HCM mutation, TNNT2 K280N, obtained from an explanted heart
Yazar:: Bayliss, C, ve diğerleri
Baskı/Yayın Bilgisi: (2012)

Familial Dilated Cardiomyopathy Caused by an Alpha-Tropomyosin Mutation: The Distinctive Natural History of Sarcomeric DCM
Yazar:: Lakdawala, N, ve diğerleri
Baskı/Yayın Bilgisi: (2009)

Cardiomyopathy-Causing Mutations in Thin Filament Regulatory Proteins Acutely Affeect Ca2+-Buffering and Ca2+-Dependent Signalling In Situ
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2013)

P123The rescue of Ca2+ cycling abnormalities conferred by HCM-causing mutations with analogues of the green tea polyphenol epigallocatechin-3-gallate.
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2014)

The HCM-associated cardiac Troponin T mutation K280N causes reduced responsiveness to protein kinase A
Yazar:: Van Der Velden, J, ve diğerleri
Baskı/Yayın Bilgisi: (2012)

Cardiomyopathy-causing mutations in cardiac thin filament regulatory proteins acutely affect Ca2+ buffering and Ca2+ dependant signalling in situ
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2012)

Comparison of the functional effects of mutations in troponin T which cause dilated and hypertrophic cardiomyopathies
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2002)

The nemaline myopathy-causing E117K mutation in β-tropomyosin reduces thin filament activation.
Yazar:: Karpicheva, O, ve diğerleri
Baskı/Yayın Bilgisi: (2013)

Mutations in fast skeletal troponin I, troponin T and beta-tropomyosin that cause distal arthrogryposis all enhance thin filament activation
Yazar:: Robinson, P, ve diğerleri
Baskı/Yayın Bilgisi: (2005)

A novel interaction between the C5 and C8 domains of myosin binding protein-C and its modulation by HCM mutations
Yazar:: Flashman, E, ve diğerleri
Baskı/Yayın Bilgisi: (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.
Yazar:: Redwood, C, ve diğerleri
Baskı/Yayın Bilgisi: (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.
Yazar:: Dass, S, ve diğerleri
Baskı/Yayın Bilgisi: (2012)

Investigation of troponin I mutations causing familial hypertrophic cardiomyopathy
Yazar:: Abdulrazzak, H, ve diğerleri
Baskı/Yayın Bilgisi: (2001)

Effects of hypertrophic cardiomyopathy mutations in troponin I on contractility of skinned cardiac muscle fibres
Yazar:: Burton, D, ve diğerleri
Baskı/Yayın Bilgisi: (2002)

Functional effects of the DCM mutant Gly159Asp troponin C in skinned muscle fibres.
Yazar:: Preston, L, ve diğerleri
Baskı/Yayın Bilgisi: (2007)

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

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