Identification and functional analysis of cardiac troponin I as a novel disease gene in autosomal dominant familial dilated cardiomyopathy

Identification and functional analysis of cardiac troponin I as a novel disease gene in autosomal dominant familial dilated cardiomyopathy

Sonraí bibleagrafaíochta
Príomhchruthaitheoirí:	Carballo, S, Redwood, C, Robinson, P, Blair, E, Watkins, H
Formáid:	Conference item
Foilsithe / Cruthaithe:	2006

Míreanna comhchosúla

Identification and functional characterization of cardiac troponin I as a novel disease gene in autosomal dominant dilated cardiomyopathy.
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A novel mutation in phospholamban causes a mixed hypertrophic and dilated cardiomyopathy phenotype with autosomal dominant inheritance
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Dilated and hypertrophic cardiomyopathy mutations in troponin and alpha-tropomyosin have opposing effects on the calcium affinity of cardiac thin filaments.
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Functional effects of mutations in troponin T and tropomyosin which cause dilated cardiomyopathy
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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.
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Comparison of the functional effects of mutations in troponin T which cause dilated and hypertrophic cardiomyopathies
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Dilated cardiomyopathy causing mutations in cardiac troponin T (TNT), cardiac troponin C (TNC), and alpha tropomyosin (TM) reduce CA(2+) sensitivity and maximum calcium activation
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Structure-function relationships of eight mutations in troponin and tropomyosin that cause dilated cardiomyopathy
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Altered inhibitory and troponin C-binding activities in cardiac troponin I mutants known to cause hypertrophic cardiomyopathy
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Investigating the Effect of Cardiomyopathy-Causing Mutations in Cardiac Troponin-T on Calcium Buffering In Situ
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The role of cardiac troponin T quantity and function in cardiac development and dilated cardiomyopathy.
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Altered regulatory properties of human cardiac troponin I mutants that cause hypertrophic cardiomyopathy.
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Using fluorescence emission spectroscopy to asses the Ca2+ affinity of reconstituted troponin and thin filaments containing cardiomyopathy causing mutations of troponin and alpha-tropomyosin
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Hypertrophic and dilated cardiomyopathycausing mutations of troponin and alpha-tropomyosin have opposite effects on thin filament calcium binding
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The effect of HCM mutations in troponin T and troponin I on the calcium binding of human cardiac troponin
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Two mutations in human cardiac troponin I known to cause hypertrophic cardiomyopathy have different effects on cardiac muscle contraction
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Novel mutations in cardiac MYBPC3 causing early onset malignant hypertrophic cardiomyopathy
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Two mutations in troponin I that cause hypertrophic cardiomyopathy have contrasting effects on cardiac muscle contractility.
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Novel mutations in cardiac MYPBC3 cause early onset malignant hypertrophic cardiomyopathy (HCM)
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Cardiac troponin I is a potential novel substrate for AMP-activated protein kinase
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Different expression and prognostic value of troponin in ischemic cardiomyopathy and non-ischemic dilated cardiomyopathy
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Long-term prognostic value of high-sensitivity cardiac troponin-I in patients with idiopathic dilated cardiomyopathy
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The effect of mutations in alpha-tropomyosin (E40K and E54K) that cause familial dilated cardiomyopathy on the regulatory mechanism of cardiac muscle thin filaments.
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