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OBSCN Mutations Associated with Dilated Cardiomyopathy and Haploinsufficiency

PloS one, 2015-09, Vol.10 (9), p.e0138568-e0138568

2015

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Quantifying the Release of Biomarkers of Myocardial Necrosis from Cardiac Myocytes and Intact Myocardium

Clinical chemistry (Baltimore, Md.), 2017-05, Vol.63 (5), p.990-996

2017

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Evidence From Human Myectomy Samples That MYBPC3 Mutations Cause Hypertrophic Cardiomyopathy Through Haploinsufficiency

Circulation research, 2009-07, Vol.105 (3), p.219-222

2009

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How do MYBPC3 mutations cause hypertrophic cardiomyopathy?

Journal of muscle research and cell motility, 2012-05, Vol.33 (1), p.75-80

2012

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Pressure Overload Is Associated With Low Levels of Troponin I and Myosin Binding Protein C Phosphorylation in the Hearts of Patients With Aortic Stenosis

Frontiers in physiology, 2020-03, Vol.11, p.241-241

2020

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Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes

Scientific reports, 2017-11, Vol.7 (1), p.14829-11, Article 14829

2017

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The Dilated Cardiomyopathy-Causing Mutation ACTC E361G in Cardiac Muscle Myofibrils Specifically Abolishes Modulation of Ca2+ Regulation by Phosphorylation of Troponin I

Biophysical journal, 2014-11, Vol.107 (10), p.2369-2380

2014

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A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation

American journal of physiology. Heart and circulatory physiology, 2016-08, Vol.311 (2), p.H465-H475

2016

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Investigations into the Sarcomeric Protein and Ca2+-Regulation Abnormalities Underlying Hypertrophic Cardiomyopathy in Cats (Felix catus)

Frontiers in physiology, 2017-06, Vol.8, p.348-348

2017

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Tropomyosin isoform expression and phosphorylation in the human heart in health and disease

Journal of muscle research and cell motility, 2013-08, Vol.34 (3-4), p.189-197

2013

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Erratum to: How do MYBPC3 mutations cause hypertrophic cardiomyopathy?

Journal of muscle research and cell motility, 2012-05, Vol.33 (1), p.81-81

2012

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Investigation of changes in skeletal muscle α-actin expression in normal and pathological human and mouse hearts

Journal of muscle research and cell motility, 2010-09, Vol.31 (3), p.207-214

2010

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Analysis of cardiac myosin binding protein-C phosphorylation in human heart muscle

Journal of molecular and cellular cardiology, 2010-12, Vol.49 (6), p.1003-1011

2010

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The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin I

Biophysical journal, 2014-11, Vol.107 (10), p.2369-2380

2014

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DCM Mutation ACTCE361G Causes Uncoupling of Myofibril Sensitivity from TnI Phosphorylation that can be Reversed by Epigallocatechin-3-Gallate

Biophysical journal, 2015-01, Vol.108 (2), p.292a-292a

2015

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Obscurin Mutations Cause Haploinsufficiency and are Common in Patients with Familial Dilated Cardiomyopathy (FDCM)

Biophysical journal, 2015-01, Vol.108 (2), p.292a-292a

2015

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Myofibrillar Ca2+ sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T

Cardiovascular research, 2013-03, Vol.97 (3), p.500-508

2013

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Myosin binding protein C phosphorylation in normal, hypertrophic and failing human heart muscle

Journal of molecular and cellular cardiology, 2008-08, Vol.45 (2), p.209-216

2008

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Investigations into the Sarcomeric Protein and Ca 2+ -Regulation Abnormalities Underlying Hypertrophic Cardiomyopathy in Cats ( Felix catus )

Frontiers in physiology, 2017, Vol.8, p.348

2017

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Dcm-Causing Mutation E361G in Actin Uncouples Myofibril Ca2+ Sensitivity from Protein Phosphorylation

Biophysical journal, 2014-01, Vol.106 (2), p.774a-775a

2014

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Molecular Mechanism of the E99K Mutation in Cardiac Actin (ACTC Gene) That Causes Apical Hypertrophy in Man and Mouse

The Journal of biological chemistry, 2011-08, Vol.286 (31), p.27582-27593

2011

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The Dilated Cardiomyopathy-Causing Mutation ACTC E361G in Cardiac Muscle Myofibrils Specifically Abolishes Modulation of Ca^sup 2+^ Regulation by Phosphorylation of Troponin I

Biophysical journal, 2014-11, Vol.107 (10), p.2369

2014

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The Dilated Cardiomyopathy-Causing Mutation ACTC E361G in Cardiac Muscle Myofibrils Specifically Abolishes Modulation of Ca 2+ Regulation by Phosphorylation of Troponin I

Biophysical journal, 2014-11, Vol.107 (10), p.2369-2380

2014

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Quantitative Analysis of MyBP-C Phosphorylation in Human Heart using Phosphate Affinity SDS-Page

Biophysical journal, 2010-01, Vol.98 (3), p.756a-756a

2010

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Myofibrillar Ca(2+) sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T

Cardiovascular research, 2013-03, Vol.97 (3), p.500

2013

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OBSCN Mutations Associated with Dilated Cardiomyopathy and Haploinsufficiency

Quantifying the Release of Biomarkers of Myocardial Necrosis from Cardiac Myocytes and Intact Myocardium

Evidence From Human Myectomy Samples That MYBPC3 Mutations Cause Hypertrophic Cardiomyopathy Through Haploinsufficiency

How do MYBPC3 mutations cause hypertrophic cardiomyopathy?

Pressure Overload Is Associated With Low Levels of Troponin I and Myosin Binding Protein C Phosphorylation in the Hearts of Patients With Aortic Stenosis

Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes

The Dilated Cardiomyopathy-Causing Mutation ACTC E361G in Cardiac Muscle Myofibrils Specifically Abolishes Modulation of Ca2+ Regulation by Phosphorylation of Troponin I

A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation

Investigations into the Sarcomeric Protein and Ca2+-Regulation Abnormalities Underlying Hypertrophic Cardiomyopathy in Cats (Felix catus)

Tropomyosin isoform expression and phosphorylation in the human heart in health and disease

Erratum to: How do MYBPC3 mutations cause hypertrophic cardiomyopathy?

Investigation of changes in skeletal muscle α-actin expression in normal and pathological human and mouse hearts

Analysis of cardiac myosin binding protein-C phosphorylation in human heart muscle

The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin I

DCM Mutation ACTCE361G Causes Uncoupling of Myofibril Sensitivity from TnI Phosphorylation that can be Reversed by Epigallocatechin-3-Gallate

Obscurin Mutations Cause Haploinsufficiency and are Common in Patients with Familial Dilated Cardiomyopathy (FDCM)

Myofibrillar Ca2+ sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T

Myosin binding protein C phosphorylation in normal, hypertrophic and failing human heart muscle

Investigations into the Sarcomeric Protein and Ca 2+ -Regulation Abnormalities Underlying Hypertrophic Cardiomyopathy in Cats ( Felix catus )

Dcm-Causing Mutation E361G in Actin Uncouples Myofibril Ca2+ Sensitivity from Protein Phosphorylation

Molecular Mechanism of the E99K Mutation in Cardiac Actin (ACTC Gene) That Causes Apical Hypertrophy in Man and Mouse

The Dilated Cardiomyopathy-Causing Mutation ACTC E361G in Cardiac Muscle Myofibrils Specifically Abolishes Modulation of Ca^sup 2+^ Regulation by Phosphorylation of Troponin I

The Dilated Cardiomyopathy-Causing Mutation ACTC E361G in Cardiac Muscle Myofibrils Specifically Abolishes Modulation of Ca 2+ Regulation by Phosphorylation of Troponin I

Quantitative Analysis of MyBP-C Phosphorylation in Human Heart using Phosphate Affinity SDS-Page

Myofibrillar Ca(2+) sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T

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