J. Kentish

发表

The role of troponin C in modulating the Ca2+ sensitivity of mammalian skinned cardiac and skeletal muscle fibres.

S. Palmer, J. Kentish, J C Kentish, 1994, The Journal of physiology.

A model of cardiac contraction based on novel measurements of tension development in human cardiomyocytes.

C. D. dos Remedios, S. Niederer, N. Smith, 2017, Journal of molecular and cellular cardiology.

Passive Stiffness of Myocardium From Congenital Heart Disease and Implications for Diastole

Felix Chua, Efstathios Vassiliadis, T. Herron, 2010, Circulation.

The cellular basis of the length-tension relation in cardiac muscle.

D. Allen, J. Kentish, D G Allen, 1985, Journal of molecular and cellular cardiology.

Changes in force and cytosolic Ca2+ concentration after length changes in isolated rat ventricular trabeculae

J. Kentish, A. Wrzosek, J C Kentish, 1998, The Journal of physiology.

Positive force- and [Ca2+]i-frequency relationships in rat ventricular trabeculae at physiological frequencies.

J. Kentish, J. Layland, Joanne Layland, 1999, American journal of physiology. Heart and circulatory physiology.

Comparison between the Sarcomere Length‐Force Relations of Intact and Skinned Trabeculae from Rat Right Ventricle: Influence of Calcium Concentrations on These Relations

H. T. ter Keurs, M. Noble, L. Ricciardi, 1986, Circulation research.

Effect of pH on myofilament Ca(2+)-sensitivity in alpha-toxin permeabilized guinea pig detrusor muscle.

C. Fry, C. Wu, J. Kentish, 1995, The Journal of urology.

Effect of pH on Myofilament Ca sup 2 Plus -Sensitivity in Alphatoxin Permeabilized Guinea Pig Detrusor Muscle

C. Fry, Changhao Wu, J. Kentish, 1995 .

Enhanced length-dependent Ca2+ activation in fish cardiomyocytes permits a large operating range of sarcomere lengths.

E. White, J. Kentish, S. M. Patrick, 2010, Journal of molecular and cellular cardiology.

Ca(2+)- and caffeine-induced Ca2+ release from the sarcoplasmic reticulum in rat skinned trabeculae: effects of pH and Pi.

J. Kentish, J. Xiang, 1997, Cardiovascular research.

Is force production in the myocardium directly dependent upon the free energy change of ATP hydrolysis?

D. Allen, J. Kentish, 1986, Journal of molecular and cellular cardiology.

Novel Role for p90 Ribosomal S6 Kinase in the Regulation of Cardiac Myofilament Phosphorylation*

E. Ehler, S. Sadayappan, J. Kentish, 2010, The Journal of Biological Chemistry.

Calcium release from cardiac sarcoplasmic reticulum induced by photorelease of calcium or Ins(1,4,5)P3.

M. Ferenczi, J. Kentish, R. Barsotti, 1990, The American journal of physiology.

A role for the sarcolemmal Na(+)/H(+) exchanger in the slow force response to myocardial stretch.

J. Kentish, 1999, Circulation research.

Increased myofilament Ca2+ sensitivity and diastolic dysfunction as early consequences of Mybpc3 mutation in heterozygous knock-in mice

F. Weinberger, L. Carrier, C. Coirault, 2012, Journal of molecular and cellular cardiology.

Effects of inorganic phosphate and ADP on calcium handling by the sarcoplasmic reticulum in rat skinned cardiac muscles.

J. Kentish, J. Xiang, 1995, Cardiovascular research.

Activation of Myocardial Contraction by the N-Terminal Domains of Myosin Binding Protein-C

M. Gautel, T. Herron, E. Rostkova, 2006, Circulation research.

Monophosphorylation of cardiac troponin-I at Ser-23/24 is sufficient to regulate cardiac myofibrillar Ca2+ sensitivity and calpain-induced proteolysis

C. D. dos Remedios, Ying Ge, A. Martín-Garrido, 2018, The Journal of Biological Chemistry.

Protection against endotoxemia‐induced contractile dysfunction in mice with cardiac‐specific expression of slow skeletal troponin I

A. Shah, D. Grieve, R. Solaro, 2005, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

Transitions in isoform populations of thick and thin filament proteins and calcium activation of force and ATP hydrolysis by cardiac myofilaments.

J. Kentish, R. Solaro, A. Martin, 1989, Progress in clinical and biological research.

From genotype to phenotype: a longitudinal study of a patient with hypertrophic cardiomyopathy due to a mutation in the MYBPC3 gene

Steven B Marston, Adam M Jacques, J. Kentish, 2009, Journal of Muscle Research and Cell Motility.

Effects of Acidosis on Ventricular Muscle From Adult and Neonatal Rats

D. Allen, J. Kentish, R. Solaro, 1988, Circulation research.

Distinct Sarcomeric Substrates Are Responsible for Protein Kinase D-mediated Regulation of Cardiac Myofilament Ca2+ Sensitivity and Cross-bridge Cycling*

M. Gautel, S. Sadayappan, J. Robbins, 2009, The Journal of Biological Chemistry.

Right Ventricle Has Normal Myofilament Function But Shows Perturbations in the Expression of Extracellular Matrix Genes in Patients With Tetralogy of Fallot Undergoing Pulmonary Valve Replacement

M. Mayr, V. Tsang, C. D. dos Remedios, 2020, Journal of the American Heart Association.

cMyBP-C as a promiscuous substrate: phosphorylation by non-PKA kinases and its potential significance

J. Kentish, M. Avkiran, F. Cuello, 2011, Journal of Muscle Research and Cell Motility.

Abstract 154: Direct Activation of Type I Protein Kinase A (PKA) by Oxidants Independently of cAMP is Mediated by RI Subunit Interprotein Disulphide Bond Formation

R. Wait, J. P. Brennan, P. Eaton, 2006 .

Protein Kinase D Selectively Targets Cardiac Troponin I and Regulates Myofilament Ca 2 (cid:1) Sensitivity in Ventricular Myocytes Cellular Biology

M. Mayr, T. Wieland, S. Lutz, 2007 .

Protein Kinase D Is a Novel Mediator of Cardiac Troponin I Phosphorylation and Regulates Myofilament Function Cellular

M. Gautel, T. Herron, J. Kentish, 2004 .

Evidence that a decrease in sarcomere length reduces the Ca++ affinity of troponin in the intact cardiac myofibril

D. Allen, J. Kentish, 1987 .

Photolysis of the novel inotropes EMD 57033 and EMD 57439: evidence that Ca2+ sensitization and phosphodiesterase inhibition depend upon the same enantiomeric site

S. Palmer, J. Kentish, J. Lee, 1996, British journal of pharmacology.

Some characteristics of Ca2+- regulated force production in EGTA- treated muscles from rat heart

B. R. Jewell, J. Kentish, 1984, The Journal of general physiology.

Protein phosphatase 2A contributes to the cardiac dysfunction induced by endotoxemia

Simon J. Walker, A. Shah, J. Kentish, 2009, Cardiovascular research.

Does esmolol only act as a β-blocker? A novel mode of action at higher doses in rats: O-12

J. Kentish, D. Chambers, H. Fallouh, 2007 .

Functional Analysis of a Unique Troponin C Mutation, GLY159ASP, that Causes Familial Dilated Cardiomyopathy, Studied in Explanted Heart Muscle

D. Ward, J. Kaski, Steven B Marston, 2009, Circulation. Heart failure.

Combined inhibitory actions of acidosis and phosphate on maximum force production in rat skinned cardiac muscle

J. Kentish, 1991, Pflügers Archiv.

The effects of inorganic phosphate and creatine phosphate on force production in skinned muscles from rat ventricle.

J. Kentish, 1986, The Journal of physiology.

Phosphorylation of Troponin I by Protein Kinase A Accelerates Relaxation and Crossbridge Cycle Kinetics in Mouse Ventricular Muscle

J. Leiden, R. Solaro, S. Palmer, 2001, Circulation research.

Ca2+, pH and the regulation of cardiac myofilament force and ATPase activity

R. Solaro, J. Kentish, Saleh C. El-Salehl, 1989, Molecular and Cellular Biochemistry.

Activation and Relaxation in Rat and Guinea Pig Skinned Trabeculae 2+ and Crossbridge Kinetics in Determining the Maximum Rates of Ca 2+ Roles of Ca

S. Palmer, J. Kentish, 2013 .

Roles of Ca2+ and crossbridge kinetics in determining the maximum rates of Ca2+ activation and relaxation in rat and guinea pig skinned trabeculae.

S. Palmer, J. Kentish, J C Kentish, 1998, Circulation research.

The inhibitory effects of monovalent ions on force development in detergent‐skinned ventricular muscle from guinea‐pig.

J. Kentish, 1984, The Journal of physiology.

Direct attachment of membrane to the Z-band of rabbit skeletal myofibrils

J. Kentish, 1983, Journal of Muscle Research & Cell Motility.

Direct attachment of membrane to the rabbit skeletal myofibrils

J. Kentish, 1983 .

Effects of changes of pH on the contractile function of cardiac muscle.

J. Kentish, C. Orchard, 1990, The American journal of physiology.

Targeting for cardioplegia: arresting agents and their safety.

J. Kentish, D. Chambers, H. Fallouh, 2009, Current opinion in pharmacology.

Positive force-and [ Ca 2 1 ] i-frequency relationships in rat ventricular trabeculae at physiological frequencies

J. Kentish, J. Layland, 1998 .

Protein Kinase D Is a Novel Mediator of Cardiac Troponin I Phosphorylation and Regulates Myofilament Function

M. Gautel, T. Herron, J. Kentish, 2004, Circulation research.

cMyBP-C as a promiscuous substrate: phosphorylation by non-PKA kinases and its potential significance

J. Kentish, M. Avkiran, F. Cuello, 2012, Journal of Muscle Research and Cell Motility.

Protein Kinase D Selectively Targets Cardiac Troponin I and Regulates Myofilament Ca2+ Sensitivity in Ventricular Myocytes

M. Mayr, T. Wieland, S. Lutz, 2007, Circulation research.

The influence of pH on the Ca2+-regulated ATPase of cardiac and white skeletal myofibrils.

W. Nayler, J. Kentish, 1979, Journal of molecular and cellular cardiology.

Effect of pH on the Ca2+-dependent ATPase of rabbit cardiac and white skeletal myofibrils [proceedings].

W. Nayler, J. Kentish, 1977, The Journal of physiology.

Reduced First-Phase Ejection Fraction and Sustained Myocardial Wall Stress in Hypertensive Patients With Diastolic Dysfunction

A. Shah, P. Chowienczyk, J. Simpson, 2017, Hypertension.

Differential effects of the Ca2+ sensitizers caffeine and CGP 48506 on the relaxation rate of rat skinned cardiac trabeculae.

S. Palmer, J. Kentish, 1997, Circulation research.

Calcium concentration in the myoplasm of skinned ferret ventricular muscle following changes in muscle length.

D. Allen, J. Kentish, 1988, The Journal of physiology.

Normal passive viscoelasticity but abnormal myofibrillar force generation in human hypertrophic cardiomyopathy

H. Watkins, V. Tsang, C. D. dos Remedios, 2010, Journal of molecular and cellular cardiology.

Unloaded shortening velocities of rabbit masseter muscle fibres expressing skeletal or alpha‐cardiac myosin heavy chains.

J. Kentish, J. Sciote, 1996, The Journal of physiology.

Oxidant-induced Activation of Type I Protein Kinase A Is Mediated by RI Subunit Interprotein Disulfide Bond Formation*

R. Wait, J. P. Brennan, P. Eaton, 2006, Journal of Biological Chemistry.

On the force-length relation in myocardium

H. E. Keurs, J. Bucx, J. Kentish, 1987 .

Effects of α1‐ or β‐adrenoceptor stimulation on work‐loop and isometric contractions of isolated rat cardiac trabeculae

J. Kentish, J. Layland, 2000, The Journal of physiology.

The Contribution of Myofibrillar Properties to the Sarcomere Length-Force Relationship of Cardiac Muscle

J. C. Kentish, D. Allen, H. E. Keurs, 1988 .

Differential effects of length on maximum force production and myofibrillar ATPase activity in rat skinned cardiac muscle.

J. Kentish, G. Stienen, J C Kentish, 1994, The Journal of physiology.

Esmolol cardioplegia: the cellular mechanism of diastolic arrest.

M. Shattock, J. Kentish, L. McLatchie, 2010, Cardiovascular research.

Functional Analysis of a Unique Troponin C Mutation, GLY159ASP, that Causes Familial Dilated Cardiomyopathy, Studied in Explanted Heart Muscle

D. Ward, J. Kaski, Steven B Marston, 2009, Circulation: Heart Failure.

Positive force- and [Ca2+]i-frequency relationships in rat ventricular trabeculae at physiological frequencies.

J. Kentish, J. Layland, 1999, American journal of physiology. Heart and circulatory physiology.

The influence of monovalent cations on myofibrillar function

J. Kentish, 1983 .

Myofilament‐based relaxant effect of isoprenaline revealed during work‐loop contractions in rat cardiac trabeculae

J. Kentish, J. Layland, Jonathan C. Kentish, 2002, The Journal of physiology.

Isoprenaline reverses the slow force responses to a length change in isolated rabbit papillary muscle

J. Kentish, P. Largen, R. Davey, 1992, Pflügers Archiv.

Abstract 154: Direct Activation of Type I Protein Kinase A (PKA) by Oxidants Independently of cAMP is Mediated by RI Subunit Interprotein Disulphide Bond Formation

R. Wait, J. P. Brennan, P. Eaton, 2006 .