Contractile dysfunction irrespective of the mutant protein in human hypertrophic cardiomyopathy with normal systolic function.

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Contractile dysfunction irrespective of the mutant protein in human hypertrophic cardiomyopathy with normal systolic function. / Dijk, van; Sabine, J; Paalberends, E Rosalie; Najafi, Aref; Michels, Michelle; Carrier, Lucie; Carrier, Lucie; Boontje, Nicky M; Kuster, Diederik W D; van Slegtenhorst, Marjon; Dooijes, Dennis; Cris, Dos Remedios; Cate, Ten; Folkert, J; Stienen, Ger J M; van der Velden, Jolanda.

In: CIRC-HEART FAIL, Vol. 5, No. 1, 1, 2012, p. 36-46.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Dijk, V, Sabine, J, Paalberends, ER, Najafi, A, Michels, M, Carrier, L, Carrier, L, Boontje, NM, Kuster, DWD, van Slegtenhorst, M, Dooijes, D, Cris, DR, Cate, T, Folkert, J, Stienen, GJM & van der Velden, J 2012, 'Contractile dysfunction irrespective of the mutant protein in human hypertrophic cardiomyopathy with normal systolic function.', CIRC-HEART FAIL, vol. 5, no. 1, 1, pp. 36-46. <http://www.ncbi.nlm.nih.gov/pubmed/22178992?dopt=Citation>

APA

Dijk, V., Sabine, J., Paalberends, E. R., Najafi, A., Michels, M., Carrier, L., Carrier, L., Boontje, N. M., Kuster, D. W. D., van Slegtenhorst, M., Dooijes, D., Cris, D. R., Cate, T., Folkert, J., Stienen, G. J. M., & van der Velden, J. (2012). Contractile dysfunction irrespective of the mutant protein in human hypertrophic cardiomyopathy with normal systolic function. CIRC-HEART FAIL, 5(1), 36-46. [1]. http://www.ncbi.nlm.nih.gov/pubmed/22178992?dopt=Citation

Vancouver

Bibtex

@article{ee7dc4c3dc404f25bd3b412840fd2c95,
title = "Contractile dysfunction irrespective of the mutant protein in human hypertrophic cardiomyopathy with normal systolic function.",
abstract = "Hypertrophic cardiomyopathy (HCM), typically characterized by asymmetrical left ventricular hypertrophy, frequently is caused by mutations in sarcomeric proteins. We studied if changes in sarcomeric properties in HCM depend on the underlying protein mutation.",
keywords = "Adult, Humans, Male, Aged, Female, Middle Aged, Disease Progression, Phosphorylation, Blood Pressure/physiology, Ventricular Function, Left/*physiology, Systole/physiology, Mutation/*genetics, Calcium/physiology, Cardiomyopathy, Hypertrophic/*genetics/pathology/*physiopathology, Carrier Proteins/*genetics, Cyclic AMP-Dependent Protein Kinases/pharmacology, Diastole/physiology, Myocardial Contraction/*physiology, Sarcomeres/drug effects/physiology, Adult, Humans, Male, Aged, Female, Middle Aged, Disease Progression, Phosphorylation, Blood Pressure/physiology, Ventricular Function, Left/*physiology, Systole/physiology, Mutation/*genetics, Calcium/physiology, Cardiomyopathy, Hypertrophic/*genetics/pathology/*physiopathology, Carrier Proteins/*genetics, Cyclic AMP-Dependent Protein Kinases/pharmacology, Diastole/physiology, Myocardial Contraction/*physiology, Sarcomeres/drug effects/physiology",
author = "van Dijk and J Sabine and Paalberends, {E Rosalie} and Aref Najafi and Michelle Michels and Lucie Carrier and Lucie Carrier and Boontje, {Nicky M} and Kuster, {Diederik W D} and {van Slegtenhorst}, Marjon and Dennis Dooijes and Cris, {Dos Remedios} and Ten Cate and J Folkert and Stienen, {Ger J M} and {van der Velden}, Jolanda",
year = "2012",
language = "English",
volume = "5",
pages = "36--46",
journal = "CIRC-HEART FAIL",
issn = "1941-3289",
publisher = "LIPPINCOTT WILLIAMS & WILKINS",
number = "1",

}

RIS

TY - JOUR

T1 - Contractile dysfunction irrespective of the mutant protein in human hypertrophic cardiomyopathy with normal systolic function.

AU - Dijk, van

AU - Sabine, J

AU - Paalberends, E Rosalie

AU - Najafi, Aref

AU - Michels, Michelle

AU - Carrier, Lucie

AU - Carrier, Lucie

AU - Boontje, Nicky M

AU - Kuster, Diederik W D

AU - van Slegtenhorst, Marjon

AU - Dooijes, Dennis

AU - Cris, Dos Remedios

AU - Cate, Ten

AU - Folkert, J

AU - Stienen, Ger J M

AU - van der Velden, Jolanda

PY - 2012

Y1 - 2012

N2 - Hypertrophic cardiomyopathy (HCM), typically characterized by asymmetrical left ventricular hypertrophy, frequently is caused by mutations in sarcomeric proteins. We studied if changes in sarcomeric properties in HCM depend on the underlying protein mutation.

AB - Hypertrophic cardiomyopathy (HCM), typically characterized by asymmetrical left ventricular hypertrophy, frequently is caused by mutations in sarcomeric proteins. We studied if changes in sarcomeric properties in HCM depend on the underlying protein mutation.

KW - Adult

KW - Humans

KW - Male

KW - Aged

KW - Female

KW - Middle Aged

KW - Disease Progression

KW - Phosphorylation

KW - Blood Pressure/physiology

KW - Ventricular Function, Left/physiology

KW - Systole/physiology

KW - Mutation/genetics

KW - Calcium/physiology

KW - Cardiomyopathy, Hypertrophic/genetics/pathology/physiopathology

KW - Carrier Proteins/genetics

KW - Cyclic AMP-Dependent Protein Kinases/pharmacology

KW - Diastole/physiology

KW - Myocardial Contraction/physiology

KW - Sarcomeres/drug effects/physiology

KW - Adult

KW - Humans

KW - Male

KW - Aged

KW - Female

KW - Middle Aged

KW - Disease Progression

KW - Phosphorylation

KW - Blood Pressure/physiology

KW - Ventricular Function, Left/physiology

KW - Systole/physiology

KW - Mutation/genetics

KW - Calcium/physiology

KW - Cardiomyopathy, Hypertrophic/genetics/pathology/physiopathology

KW - Carrier Proteins/genetics

KW - Cyclic AMP-Dependent Protein Kinases/pharmacology

KW - Diastole/physiology

KW - Myocardial Contraction/physiology

KW - Sarcomeres/drug effects/physiology

M3 - SCORING: Journal article

VL - 5

SP - 36

EP - 46

JO - CIRC-HEART FAIL

JF - CIRC-HEART FAIL

SN - 1941-3289

IS - 1

M1 - 1

ER -