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American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 01/1999, Volume 276, Issue 1, p. H18
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2012, Volume 52, Issue 6, pp. 1299 - 1307
Abstract Hypertrophic cardiomyopathy (HCM) is frequently caused by mutations in MYBPC3 encoding cardiac myosin-binding protein C (cMyBP-C). The mechanisms... 
Cardiovascular | Diastolic dysfunction | Ca2+ sensitivity | Ca2+ transient | Mouse model | Hypertrophy | MYOCARDIUM | BINDING-PROTEIN-C | CARDIAC & CARDIOVASCULAR SYSTEMS | FAMILIAL HYPERTROPHIC CARDIOMYOPATHY | UBIQUITIN-PROTEASOME SYSTEM | MYOCYTES | PHOSPHORYLATION | MECHANISMS | CELL BIOLOGY | GENE | MESSENGER-RNA DECAY | EXPRESSION | Cardiomyopathy, Hypertrophic - genetics | Echocardiography | Diastole | Calcium - metabolism | Cardiomyopathy, Hypertrophic - metabolism | Mice, Transgenic | Gene Knock-In Techniques | Carrier Proteins - genetics | Animals | Heart Ventricles - physiopathology | Cardiomyopathy, Hypertrophic - physiopathology | Myocytes, Cardiac - metabolism | Heterozygote | Heart Ventricles - metabolism | Mice | Myofibrils - metabolism | Mutation | Gene Order | cTnI, cardiac troponin I | Mybpc3, mouse cardiac myosin-binding protein C gene | PKA, cAMP-dependent protein kinase A | max F, maximal Ca2+-activated force | KI, homozygous Mybpc3-targeted knock-in mice | MYBPC3, human cardiac myosin-binding protein C gene | Het, heterozygous Mybpc3-targeted knock-in mice | PLB, phospholamban | KO, homozygous Mybpc3-targeted knock-out mice | Ca2+ exchanger | SERCA2, SR-Ca2+ ATPase | HCM, hypertrophic cardiomyopathy | NCX, Na+ | SL, sarcomere length | SR, sarcoplasmic reticulum | cMyBP-C, cardiac myosin-binding protein C | nH, Hill coefficient | pCa50, log of [Ca2+] required for 50% of maximal activation | LVH, left ventricular hypertrophy | CSQ, calsequestrin | Original
Journal Article
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 05/2010, Volume 48, Issue 5, p. 917
Fish myocytes continue to develop active tension when stretched to sarcomere lengths (SLs) on the descending limb of the mammalian length-tension relationship.... 
Myosin | Physiological aspects | Protein C | Universities and colleges | Muscle proteins | Protein binding
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 06/2012, Volume 52, Issue 6, pp. 1299 - 1307
Hypertrophic cardiomyopathy (HCM) is frequently caused by mutations in MYBPC3 encoding cardiac myosin-binding protein C (cMyBP-C). The mechanisms leading from... 
Diastolic dysfunction | Mouse model | sensitivity | transient | Hypertrophy
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2011, Volume 286, Issue 7, pp. 5300 - 5310
In myocardium, the 90-kDa ribosomal S6 kinase (RSK) is activated by diverse stimuli and regulates the sarcolemmal Na+/H+ exchanger through direct... 
Antibodies
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 2018, Volume 293, Issue 22, pp. 8588 - 8599
The acceleration of myocardial relaxation produced by -adrenoreceptor stimulation is mediated in part by protein kinase A (PKA)-mediated phosphorylation of... 
MYOCARDIUM | BINDING-PROTEIN-C | MYOSIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | CARDIOMYOPATHY | MUSCLE | FAILING HUMAN HEART | KINASE-D | Ca2+ sensitivity | protein kinase D (PKD) | sarcomere | PHOSPHORYLATION SITE | myofibril | calpain | troponin | AFFINITY | cardiomyocyte | phosphorylation | cardiac muscle | MYOFILAMENT FUNCTION | Signal Transduction
Journal Article
Circulation Research, ISSN 0009-7330, 11/2004, Volume 95, Issue 11, pp. 1091 - 1099
Protein kinase D (PKD) is a serine kinase whose myocardial substrates are unknown. Yeast 2-hybrid screening of a human cardiac library, using the PKD catalytic... 
Cardiac troponin I | Calcium sensitivity | Protein phosphorylation | Protein kinase D | Contractile function | Crossbridge cycling kinetics | C FAMILY | contractile function | SARCOMERIC M-BAND | CARDIAC & CARDIOVASCULAR SYSTEMS | ATPASE ACTIVITY | RAT | MUSCLE | protein phosphorylation | cardiac troponin I | calcium sensitivity | POWER OUTPUT | protein kinase D | PERIPHERAL VASCULAR DISEASE | MOLECULAR-CLONING | crossbridge cycling kinetics | HEMATOLOGY | PHORBOL ESTERS | SIGNAL-TRANSDUCTION PATHWAY | MYOSIN-BINDING | Protein Kinase C - genetics | Phosphorylation | Connectin | Rats, Wistar | Humans | Middle Aged | Myocardial Contraction - physiology | DNA, Complementary - genetics | Molecular Sequence Data | Substrate Specificity | Male | Structure-Activity Relationship | Recombinant Fusion Proteins - metabolism | Protein Kinase C - metabolism | Troponin I - genetics | Myocardium - metabolism | Muscle Proteins - metabolism | Adult | Isometric Contraction | Calcium Signaling | Cyclic AMP-Dependent Protein Kinases - metabolism | Amino Acid Sequence | Actin Cytoskeleton - metabolism | Mutagenesis, Site-Directed | Rats | Protein Processing, Post-Translational - physiology | Phosphoserine - analysis | Two-Hybrid System Techniques | Animals | Carrier Proteins - metabolism | Myocytes, Cardiac - metabolism | Troponin I - chemistry | Troponin I - metabolism | Amino Acid Substitution
Journal Article
Journal Article
Circulation Research, ISSN 0009-7330, 03/2007, Volume 100, Issue 6, pp. 864 - 873
Journal Article
Circulation, ISSN 0009-7322, 03/2010, Volume 121, Issue 8, pp. 979 - 988
Background-In ventricular dilatation or hypertrophy, an elevated end-diastolic pressure is often assumed to be secondary to increased myocardial stiffness, but... 
Heart defects | Pressure overload | Volume overload | Congenital | Diastole | Titin | volume overload | heart defects | PRESSURE-VOLUME | CARDIAC & CARDIOVASCULAR SYSTEMS | CONTRACTILE PROPERTIES | CARDIAC MYOCYTES | RESTING TENSION | LEFT-VENTRICLE | congenital | DILATED CARDIOMYOPATHY | pressure overload | MECHANICAL-PROPERTIES | titin | MUSCLE-FIBERS | PERIPHERAL VASCULAR DISEASE | TITIN ISOFORMS | SARCOMERE LENGTHS | diastole | Protein Kinases - metabolism | Connectin | Heart Diseases - metabolism | Humans | Middle Aged | Child, Preschool | Extracellular Matrix - metabolism | Dilatation, Pathologic - physiopathology | Infant | Male | Heart Diseases - congenital | Dilatation, Pathologic - metabolism | Elasticity - physiology | Young Adult | Myocardium - metabolism | Muscle Proteins - metabolism | Adult | Female | Child | Heart - physiopathology | Heart Diseases - physiopathology | Hypertrophy, Left Ventricular - metabolism | Myocardium - pathology | Diastole - physiology | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - metabolism | Collagen - metabolism | Biopsy | Adolescent | Aged | Hypertrophy, Left Ventricular - physiopathology | Complications and side effects | Cardiomyopathy | Physiological aspects | Extracellular matrix | Congenital heart disease | Diastole (Cardiac cycle) | Research | Heart diseases | Risk factors
Journal Article
Circulation Research: Journal of the American Heart Association, ISSN 0009-7330, 05/2001, Volume 88, Issue 10, pp. 1059 - 1065
Journal Article