C. Redwood

发表

Identification and Functional Characterization of Cardiac Troponin I As a Novel Disease Gene in Autosomal Dominant Dilated Cardiomyopathy

D. Fatkin, H. Watkins, E. Blair, 2009, Circulation research.

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

H. Watkins, V. Tsang, W. McKenna, 2009, Circulation research.

Inherited cardiomyopathies.

H. Watkins, C. Redwood, Hugh Watkins, 2011, The New England journal of medicine.

The Effect of Mutations in α-Tropomyosin (E40K and E54K) That Cause Familial Dilated Cardiomyopathy on the Regulatory Mechanism of Cardiac Muscle Thin Filaments*

H. Watkins, Steven B Marston, P. Robinson, 2007, Journal of Biological Chemistry.

Localisation of AMPK γ subunits in cardiac and skeletal muscles

H. Watkins, C. Redwood, K. Pintér, 2013, Journal of Muscle Research and Cell Motility.

Chapter 6 A novel HCM mutation in cardiac troponin T primarily alters cross-bridge kinetics and increases the energetic cost of tension generation in human cardiac tissue

C. Poggesi, Steven B Marston, C. Redwood, 2014 .

Chronic Activation of γ 2 AMPK Induces Obesity and Reduces Beta Cell Function

Robin J. W. Willows, Jonathan, Parvathy E. Harikumar, 2016 .

Molecular Mechanisms of the Deregulation of Muscle Contraction Induced by the R90P Mutation in Tpm3.12 and the Weakening of This Effect by BDM and W7

C. Redwood, Y. Borovikov, D. Andreeva, 2021, International journal of molecular sciences.

Molecular mechanisms of dysfunction of muscle fibres associated with Glu139 deletion in TPM2 gene

C. Redwood, Y. Borovikov, S. V. Avrova, 2017, Scientific Reports.

AMP-Activated Protein Kinase Phosphorylates Cardiac Troponin I and Alters Contractility of Murine Ventricular Myocytes

H. Watkins, D. Carling, Ying Ge, 2012, Circulation research.

Identification of functioning regulatory sites and a new myosin binding site in the C-terminal 288 amino acids of caldesmon expressed from a human clone

M. Tanner, N. Avent, Steven B Marston, 1993, Journal of Muscle Research and Cell Motility.

Gly126Arg substitution causes anomalous behaviour of α-skeletal and β-smooth tropomyosins during the ATPase cycle.

C. Redwood, D. Levitsky, Y. Borovikov, 2014, Archives of biochemistry and biophysics.

The nemaline myopathy-causing E117K mutation in β-tropomyosin reduces thin filament activation.

P. Robinson, C. Redwood, Y. Borovikov, 2013, Archives of biochemistry and biophysics.

Modulation of the effects of tropomyosin on actin and myosin conformational changes by troponin and Ca2+.

C. Redwood, Y. Borovikov, S. V. Avrova, 2009, Biochimica et biophysica acta.

Mutations in fast skeletal troponin I, troponin T, and β‐tropomyosin that cause distal arthrogryposis all increase contractile function

H. Watkins, P. Robinson, C. Redwood, 2007, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

A revised method of troponin exchange in permeabilised cardiac trabeculae using vanadate: functional consequences of a HCM-causing mutation in troponin I

H. Watkins, C. Redwood, Laura C. Preston, 2006, Journal of Muscle Research & Cell Motility.

Aberrant developmental titin splicing and dysregulated sarcomere length in Thymosin β4 knockout mice

M. Lythgoe, A. Price, A. Taylor, 2017, Journal of molecular and cellular cardiology.

Does extracellular cardiac troponin I play a pathogenic role independently of autoantibodies?

C. Redwood, 2016, Clinical science.

Fluorescent PSC-Derived Cardiomyocyte Reporter Lines: Generation Approaches and Their Applications in Cardiovascular Medicine

B. Davies, C. Redwood, K. Gehmlich, 2020, Biology.

Mutations in the gamma(2) subunit of AMP-activated protein kinase cause familial hypertrophic cardiomyopathy: evidence for the central role of energy compromise in disease pathogenesis.

H. Watkins, J. Broxholme, B. Kerr, 2001, Human molecular genetics.

Subunit composition of AMPK trimers present in the cytokinetic apparatus: Implications for drug target identification

A. Jefferson, H. Watkins, C. Redwood, 2012, Cell cycle.

Embryonic expression of AMPK γ subunits and the identification of a novel γ2 transcript variant in adult heart

H. Watkins, C. Redwood, G. Czibik, 2012, Journal of molecular and cellular cardiology.

Determination of AMP-activated protein kinase phosphorylation sites in recombinant protein expressed using the pET28a vector: A cautionary tale

H. Watkins, D. Carling, C. Redwood, 2009, Protein expression and purification.

Monogenic causes of cardiac hypertrophy: hypertrophic cardiomyopathy and related phenotypes

H. Watkins, C. Redwood, 2005 .

Two mutations in troponin I that cause hypertrophic cardiomyopathy have contrasting effects on cardiac muscle contractility.

H. Watkins, Steven B Marston, C. Redwood, 2002, The Biochemical journal.

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*

H. Watkins, Steven B Marston, P. Robinson, 2002, The Journal of Biological Chemistry.

Physiological regulation of eukaryotic topoisomerase II.

N. J. Wells, I. Hickson, M. Sandri, 1998, Biochimica et biophysica acta.

GSK3&bgr; Phosphorylates Newly Identified Site in the Proline-Alanine–Rich Region of Cardiac Myosin–Binding Protein C and Alters Cross-Bridge Cycling Kinetics in Human: Short Communication

Jeroen A. A. Demmers, C. D. dos Remedios, S. Sadayappan, 2012, Circulation research.

Myosin Sequestration Regulates Sarcomere Function, Cardiomyocyte Energetics, and Metabolism, Informing the Pathogenesis of Hypertrophic Cardiomyopathy

J. F. Staples, E. Ashley, S. Colan, 2020, Circulation.

Mutant Muscle LIM Protein C58G causes cardiomyopathy through protein depletion

H. Watkins, A. Goel, B. Davies, 2018, Journal of molecular and cellular cardiology.

Measurement of Myofilament-Localized Calcium Dynamics in Adult Cardiomyocytes and the Effect of Hypertrophic Cardiomyopathy Mutations

Connor N Broyles, Matthew J. Daniels, H. Watkins, 2019, Circulation research.

Calcium Dynamics in Adult Cardiomyocytes and the Effect of Hypertrophic Cardiomyopathy

Connor N Broyles, Matthew J. Daniels, H. Watkins, 2022 .

Defective inhibitory properties of human cardiac troponin I mutants that cause familial hypertrophic cardiomyopathy (FHC)

H. Watkins, C. Redwood, K. Elliott, 1998 .

Severe disease expression of cardiac troponin C and T mutations in patients with idiopathic dilated cardiomyopathy.

H. Watkins, P. Elliott, J. Mogensen, 2004, Journal of the American College of Cardiology.

Dilated cardiomyopathy mutations in alpha-tropomyosin inhibit its movement during the ATPase cycle.

P. Robinson, C. Redwood, Y. Borovikov, 2009, Biochemical and biophysical research communications.

The homozygous K280N troponin T mutation alters cross-bridge kinetics and energetics in human HCM

A. Biggeri, D. Ward, C. D. dos Remedios, 2018, The Journal of general physiology.

MYBPC3 Mutations cause Hypertrophic Cardiomyopathy by Dysregulating Myosin: Implications for Therapy

J. Seidman, H. Watkins, C. Seidman, 2018, bioRxiv.

Title : Hypertrophic Cardiomyopathy Mutations in MYBPC 3 Dysregulate Myosin : Implications for Therapy

J. Seidman, H. Watkins, H. Wakimoto, 2018 .

Investigation of a transgenic mouse model of familial dilated cardiomyopathy.

K. Clarke, M. Ferenczi, S. Harding, 2010, Journal of molecular and cellular cardiology.

University of Birmingham Mammalian 2 AMPK regulates intrinsic heart rate

D. Paterson, O. Wolkenhauer, E. Lakatta, 2017 .

Chronic Activation of g 2 AMPK Induces Obesity and Reduces b Cell Function

Robin J. W. Willows, Parvathy E. Harikumar, Nathan R. Qi, 2016 .

Functional effects of the DCM mutant Gly159Asp Troponin C in skinned muscle fibres

H. Watkins, J. Mogensen, W. McKenna, 2007, Pflügers Archiv - European Journal of Physiology.

Disease modeling of a mutation in α‐actinin 2 guides clinical therapy in hypertrophic cardiomyopathy

Jussi T. Koivumäki, D. Catalucci, M. Spohn, 2019, EMBO molecular medicine.

Dilated Cardiomyopathy Mutations in Three Thin Filament Regulatory Proteins Result in a Common Functional Phenotype*

H. Watkins, J. Mogensen, W. McKenna, 2005, Journal of Biological Chemistry.

Hypertrophic cardiomyopathy mutations increase myofilament Ca 2 (cid:2) buffering, alter intracellular Ca 2 (cid:2) handling, and stimulate Ca 2 (cid:2) -dependent signaling

H. Watkins, A. Sparrow, B. Casadei, 2018 .

Evaluation of MYBPC3 trans-Splicing and Gene Replacement as Therapeutic Options in Human iPSC-Derived Cardiomyocytes

O. Müller, L. Carrier, C. Redwood, 2017, Molecular therapy. Nucleic acids.

Analysis of Contractile Function of Permeabilized Human Hypertrophic Cardiomyopathy Multicellular Heart Tissue

L. Carrier, C. Redwood, F. Friedrich, 2019, Front. Physiol..

RAPID REPORT Cardiac Excitation and Contraction Mavacamten rescues increased myoﬁlament calcium sensitivity and dysregulation of Ca 2 (cid:2) ﬂux caused by thin ﬁlament hypertrophic cardiomyopathy mutations

H. Watkins, A. Sparrow, P. Robinson, 2020 .

Human DNA topoisomerases IIα and IIβ can functionally substitute for yeastTOP2 in chromosome segregation and recombination

I. Hickson, J. Jenkins, C. Redwood, 1996, Molecular and General Genetics MGG.

Effect of hypertrophic cardiomyopathy mutations in human cardiac muscle alpha -tropomyosin (Asp175Asn and Glu180Gly) on the regulatory properties of human cardiac troponin determined by in vitro motility assay.

H. Watkins, G. Esposito, Steven B Marston, 2000, Journal of molecular and cellular cardiology.

Low expression of the K280N TNNT2 mutation is sufficient to increase basal myofilament activation in human hypertrophy cardiomyopathy

C. D. dos Remedios, B. Knollmann, C. Redwood, 2022, Journal of molecular and cellular cardiology plus.

MyBP-C Role in Thick Filament Formation Binding to the Light Meromyosin Region of the Myosin

H. Watkins, J. Moolman-Smook, E. Flashman, 2004 .

The essential role of tropomyosin in cooperative regulation of smooth muscle thin filament activity by caldesmon.

Steven B Marston, C. Redwood, 1993, The Journal of biological chemistry.

Casein Kinase II Stabilizes the Activity of Human Topoisomerase IIα in a Phosphorylation-independent Manner*

N. J. Wells, I. Hickson, A. Fry, 1998, The Journal of Biological Chemistry.

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

D. Ward, C. D. dos Remedios, W. McKenna, 2013, Cardiovascular research.

Phosphorylation of aorta caldesmon by endogeneous proteolytic fragments of protein kinase C

J. H. Collins, A. Vorotnikov, N. Gusev, 1994, Journal of Muscle Research & Cell Motility.

Ascertainment strategies and genotype:phenotype correlations in hypertrophic cardiomyopathy.

H. Watkins, E. Blair, C. Redwood, 2003, Circulation.

Molecular Mechanisms of Muscle Weakness Associated with E173A Mutation in Tpm3.12. Troponin Ca2+ Sensitivity Inhibitor W7 Can Reduce the Damaging Effect of This Mutation

C. Redwood, Y. Borovikov, S. V. Avrova, 2020, International journal of molecular sciences.

The Primary Causes of Muscle Dysfunction Associated with the Point Mutations in Tpm3.12; Conformational Analysis of Mutant Proteins as a Tool for Classification of Myopathies

C. Redwood, Y. Borovikov, S. V. Avrova, 2018, International journal of molecular sciences.

Aberrant movement of β-tropomyosin associated with congenital myopathy causes defective response of myosin heads and actin during the ATPase cycle.

C. Redwood, Y. Borovikov, S. V. Avrova, 2015, Archives of biochemistry and biophysics.

Reduced Phospholamban Phosphorylation Is Associated With Impaired Relaxation in Left Ventricular Myocytes From Neuronal NO Synthase–Deficient Mice

E. Kranias, B. Casadei, C. Sears, 2008, Circulation research.

Mavacamten rescues increased myofilament calcium sensitivity and dysregulation of Ca2+ flux caused by thin filament hypertrophic cardiomyopathy mutations

Matthew J. Daniels, H. Watkins, A. Sparrow, 2020, American journal of physiology. Heart and circulatory physiology.

The effect of the dilated cardiomyopathy-causing mutation Glu54Lys of alpha-tropomyosin on actin-myosin interactions during the ATPase cycle.

P. Robinson, C. Redwood, Y. Borovikov, 2009, Archives of biochemistry and biophysics.

Synchronous in situ ATPase activity, mechanics, and Ca2+ sensitivity of human and porcine myocardium.

P. J. Griffiths, H. Watkins, C. Redwood, 2009, Biophysical journal.

Measurement of myofilament calcium in living cardiomyocytes using a targeted genetically encoded indicator

Connor N Broyles, Matthew J. Daniels, H. Watkins, 2018, bioRxiv.

Altered contractile mechanics and Ca2+ handling contribute to cardiomyopathy pathogenesis

C. Redwood, 2015 .

The molecular anatomy of caldesmon.

Steven B Marston, C. Redwood, 1991, The Biochemical journal.

The functional effects of mutations Thr 673 → Asp and Ser702 → Asp at the Pro‐directed kinase phosophorylation sites in the C‐terminus of chicken gizzard caldesmon

N. Gusev, Steven B Marston, C. Redwood, 1993, FEBS letters.

Identification of casein kinase II as a major endogeneous caldesmon kinase in sheep aorta smooth muscle

J. H. Collins, A. Vorotnikov, N. Gusev, 1993, FEBS letters.

The functional properties of full length and mutant chicken gizzard smooth muscle caldesmon expressed in Escherichia coli

J. Bryan, Steven B Marston, C. Redwood, 1990, FEBS letters.

Modulation of thin filament activation by breakdown or isoform switching of thin filament proteins: physiological and pathological implications.

Steven B Marston, C. Redwood, 2003, Circulation research.

Looking for Targets to Restore the Contractile Function in Congenital Myopathy Caused by Gln147Pro Tropomyosin

C. Redwood, Y. Borovikov, A. O. Simonyan, 2020, International journal of molecular sciences.

The effect of the Asp175Asn and Glu180Gly TPM1 mutations on actin-myosin interaction during the ATPase cycle.

C. Redwood, Y. Borovikov, N. Rysev, 2012, Biochimica et biophysica acta.

Hypertrophic cardiomyopathy-causing Asp175asn and Glu180gly Tpm1 mutations shift tropomyosin strands further towards the open position during the ATPase cycle.

C. Redwood, Y. Borovikov, N. Rysev, 2011, Biochemical and biophysical research communications.

Effects of two hypertrophic cardiomyopathy mutations in alpha-tropomyosin, Asp175Asn and Glu180Gly, on Ca2+ regulation of thin filament motility.

H. Watkins, G. Esposito, Steven B Marston, 1997, Biochemical and biophysical research communications.

Cardiac Myosin Binding Protein C: Its Role in Physiology and Disease

H. Watkins, J. Moolman-Smook, E. Flashman, 2004, Circulation research.

Investigation of a truncated cardiac troponin T that causes familial hypertrophic cardiomyopathy: Ca(2+) regulatory properties of reconstituted thin filaments depend on the ratio of mutant to wild-type protein.

H. Watkins, G. Esposito, Steven B Marston, 2000, Circulation research.

Myopathy-causing Q147P TPM2 mutation shifts tropomyosin strands further towards the open position and increases the proportion of strong-binding cross-bridges during the ATPase cycle.

C. Redwood, N. Kuleva, Y. Borovikov, 2016, Biochimica et biophysica acta.

The E117K mutation in β-tropomyosin disturbs concerted conformational changes of actomyosin in muscle fibers.

C. Redwood, Y. Borovikov, O. Karpicheva, 2014, Archives of biochemistry and biophysics.

Alpha-tropomyosin mutations in inherited cardiomyopathies

P. Robinson, C. Redwood, 2013, Journal of Muscle Research and Cell Motility.

The effect of the dilated cardiomyopathy-causing Glu40Lys TPM1 mutation on actin-myosin interactions during the ATPase cycle.

P. Robinson, C. Redwood, Y. Borovikov, 2011, Biochemical and biophysical research communications.

Familial dilated cardiomyopathy caused by an alpha-tropomyosin mutation: the distinctive natural history of sarcomeric dilated cardiomyopathy.

Birgit Funke, Christine E Seidman, S. Colan, 2010, Journal of the American College of Cardiology.

Dilated and Hypertrophic Cardiomyopathy Mutations in Troponin and &agr;-Tropomyosin Have Opposing Effects on the Calcium Affinity of Cardiac Thin Filaments

P. J. Griffiths, H. Watkins, P. Robinson, 2007, Circulation research.

Properties of mutant contractile proteins that cause hypertrophic cardiomyopathy.

H. Watkins, J. Moolman-Smook, C. Redwood, 1999, Cardiovascular Research.

Support for a trimeric collar of myosin binding protein C in cardiac and fast skeletal muscle, but not in slow skeletal muscle

H. Watkins, J. Moolman-Smook, E. Flashman, 2008, FEBS letters.

Identification of Novel Interactions Between Domains of Myosin Binding Protein-C That Are Modulated by Hypertrophic Cardiomyopathy Missense Mutations

H. Watkins, J. Moolman-Smook, V. Corfield, 2002, Circulation research.

Mutations in troponin T associated with Hypertrophic Cardiomyopathy increase Ca2+-sensitivity and suppress the modulation of Ca2+-sensitivity by troponin I phosphorylation☆

D. Ward, C. D. dos Remedios, M. Papadaki, 2016, Archives of biochemistry and biophysics.

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

K. Clarke, L. Monserrat, S. Harding, 2011, The Journal of Biological Chemistry.

Genetics Matters: Voyaging from the Past into the Future of Humanity and Sustainability

K. Chua, J. Harikrishna, S. Nath, 2022, International journal of molecular sciences.

Localization of the binding site of the C-terminal domain of cardiac myosin-binding protein-C on the myosin rod.

H. Watkins, E. Flashman, C. Redwood, 2007, Biochemical Journal.

Mutations of the Light Meromyosin Domain of the &bgr;-Myosin Heavy Chain Rod in Hypertrophic Cardiomyopathy

H. Watkins, J. Moolman-Smook, P. Brink, 2002, Circulation research.

Dilated cardiomyopathy mutations in thin-filament regulatory proteins reduce contractility, suppress systolic Ca2+, and activate NFAT and Akt signaling

H. Watkins, A. Sparrow, B. Casadei, 2020, American journal of physiology. Heart and circulatory physiology.

Hypertrophic cardiomyopathy mutations in MYBPC3 dysregulate myosin

Christine E Seidman, Sakthivel Sadayappan, J. Seidman, 2019, Science Translational Medicine.

Abstract 571: MYBPC3 Mutations Cause Hypertrophic Cardiomyopathy by Dysregulating Myosin: Implications for Therapy

J. Seidman, H. Watkins, C. Seidman, 2018, Circulation Research.

Hypertrophic cardiomyopathy mutations increase myofilament Ca2+ buffering, alter intracellular Ca2+ handling, and stimulate Ca2+-dependent signaling

H. Watkins, A. Sparrow, B. Casadei, 2018, The Journal of Biological Chemistry.

DCM troponin C mutant Gly159Asp blunts the response to troponin phosphorylation.

C. Redwood, C. Ashley, Laura C. Preston, 2007, Biochemical and biophysical research communications.

Conserved Noncanonical Residue Gly-126 Confers Instability to the Middle Part of the Tropomyosin Molecule*

Yaroslav A. Kainov, C. Redwood, O. Nikolaeva, 2011, The Journal of Biological Chemistry.

Effect of mutation Arg91Gly on the thermal stability of β-tropomyosin

C. Redwood, D. Levitsky, I. Nevzorov, 2008 .

Paracrine signalling by cardiac calcitonin controls atrial fibrogenesis and arrhythmia

M. Mayr, N. Ashley, A. Mead, 2020, Nature.

A mutant tropomyosin that causes hypertrophic cardiomyopathy is expressed in vivo and associated with an increased calcium sensitivity.

B. Maron, H. Watkins, C. Reggiani, 1998, Circulation research.

Mammalian γ2 AMPK regulates intrinsic heart rate

D. Paterson, O. Wolkenhauer, E. Lakatta, 2017, Nature Communications.

Mutation analysis of AMP-activated protein kinase subunits in inherited cardiomyopathies: implications for kinase function and disease pathogenesis.

H. Watkins, E. Blair, C. Redwood, 2003, Journal of molecular and cellular cardiology.

Fumarate Is Cardioprotective via Activation of the Nrf2 Antioxidant Pathway

Alan J. Robinson, Stefan Neubauer, Mark R. Viant, 2012, Cell metabolism.

Molecular Mechanisms of Deregulation of Muscle Contractility Caused by the R168H Mutation in TPM3 and Its Attenuation by Therapeutic Agents

C. Redwood, Y. Borovikov, S. V. Avrova, 2023, International journal of molecular sciences.

The molecular mechanisms of a high Ca2+-sensitivity and muscle weakness associated with the Ala155Thr substitution in Tpm3.12.

C. Redwood, Y. Borovikov, S. V. Avrova, 2019, Biochemical and biophysical research communications.

The Effect of the Arg91Gly and Glu139del Mutations in β-Tropomyosin Associated with Congenital Myopathy of Human Skeletal Muscles on Actin–Myosin Interaction

C. Redwood, Y. Borovikov, V. V. Sirenko, 2018 .

The reason for a high Ca2+-sensitivity associated with Arg91Gly substitution in TPM2 gene is the abnormal behavior and high flexibility of tropomyosin during the ATPase cycle.

C. Redwood, Y. Borovikov, S. V. Avrova, 2017, Biochemical and biophysical research communications.

Molecular mechanisms of dysfunction of muscle fibres associated with Glu139 deletion in TPM2 gene

C. Redwood, Y. Borovikov, S. V. Avrova, 2017, Scientific Reports.

Hypertrophic cardiomyopathy:a paradigm for myocardial energy depletion.

H. Watkins, E. Blair, C. Redwood, 2003, Trends in genetics : TIG.

Changes in the cardiac metabolome caused by perhexiline treatment in a mouse model of hypertrophic cardiomyopathy.

J. W. Allwood, W. Dunn, L. Carrier, 2015, Molecular bioSystems.

Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function

Robin J. W. Willows, Parvathy E. Harikumar, Nathan R. Qi, 2016, Cell Metabolism.

Molecular mechanisms of the regulation of ATPase cycle in striated muscle

C. Redwood, Y. Borovikov, O. Karpicheva, 2007 .

Calcitonin paracrine signaling controls atrial fibrogenesis and arrhythmia

M. Mayr, N. Ashley, A. Mead, 2020 .

Activation of Autophagy Ameliorates Cardiomyopathy in Mybpc3-Targeted Knockin Mice

J. Robbins, L. Carrier, C. Redwood, 2017, Circulation. Heart failure.

CalTrack

J. Seidman, H. Watkins, A. Sparrow, 2021, Circulation research.

Comparing the effects of chemical Ca2+ dyes and R-GECO on contractility and Ca2+ transients in adult and human iPSC cardiomyocytes

Connor N Broyles, Matthew J. Daniels, H. Watkins, 2023, Journal of molecular and cellular cardiology.

Crystal structure of the C1 domain of cardiac myosin binding protein-C: implications for hypertrophic cardiomyopathy.

J. Squire, N. Chayen, J. Helliwell, 2008, Journal of molecular biology.

The HCM-Associated Cardiac Troponin T Mutation K280N Increases the Energetic Cost of Tension Generation in Human Cardiac Myofibrils

C. Poggesi, L. Carrier, C. Redwood, 2013 .

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.

Localisation of AMPK γ subunits in cardiac and skeletal muscles

H. Watkins, C. Redwood, K. Pintér, 2013, Journal of Muscle Research and Cell Motility.

Ca2+ regulation of the thin filaments: biochemical mechanism and physiological role.

Steven B Marston, C. Redwood, K. Pritchard, 1988, Biochemical Society transactions.

Altered Regulatory Properties of Human Cardiac Troponin I Mutants That Cause Hypertrophic Cardiomyopathy*

H. Watkins, C. Redwood, H Watkins, 2000, The Journal of Biological Chemistry.

The Effect of the Arg91Gly and Glu139del Mutations in β-Tropomyosin Associated with Congenital Myopathy of Human Skeletal Muscles on Actin–Myosin Interaction

C. Redwood, Y. Borovikov, V. V. Sirenko, 2018, Cell and Tissue Biology.

The high Ca2+-sensitivity associated with the Glu139del and Arg91Gly mutations in tropomyosin is caused by freezing of tropomyosin near the closed position

C. Redwood, Y. Borovikov, V. V. Sirenko, 2017 .

Stability of two β-tropomyosin isoforms: effects of mutation Arg91Gly

C. Redwood, D. Levitsky, I. Nevzorov, 2009, Journal of Muscle Research and Cell Motility.

An investigation into the protonation states of the C1 domain of cardiac myosin-binding protein C.

S. Fisher, J. Squire, N. Chayen, 2008, Acta crystallographica. Section D, Biological crystallography.

The molecular mechanism of muscle dysfunction associated with the R133W mutation in Tpm2.2.

C. Redwood, Y. Borovikov, S. V. Avrova, 2019, Biochemical and biophysical research communications.

Effects of the mutation R145G in human cardiac troponin I on the kinetics of the contraction–relaxation cycle in isolated cardiac myofibrils

J. Robbins, J. James, C. Redwood, 2005, The Journal of physiology.

Evidence for haploinsufficiency as the mechanism of action of MyBP-C mutations that cause HCM

H. Watkins, S. Carballo, C. Redwood, 2008 .

Reversal of caldesmon function by anti-caldesmon antibodies confirms its role in the calcium regulation of vascular smooth muscle thin filaments.

W. Lehman, Steven B Marston, C. Redwood, 1988, Biochemical and biophysical research communications.

Binding and regulatory properties of expressed functional domains of chicken gizzard smooth muscle caldesmon.

Steven B Marston, C. Redwood, 1993, The Journal of biological chemistry.

Functional effects of hypertrophic cardiomyopathy mutations in alpha-tropomyosin on Ca2+ regulation of thm filaments

H. Watkins, G. Esposito, C. Redwood, 1998 .

New mechanisms and concepts for cardiac-resynchronization therapy.

C. Redwood, S. Neubauer, 2014, The New England journal of medicine.

MECHANISMS OF DISEASE

H. Watkins, C. Carpenter, C. Redwood, 1998 .

Disease modeling of a mutation in α‐actinin 2 guides clinical therapy in hypertrophic cardiomyopathy

Jussi T. Koivumäki, D. Catalucci, M. Spohn, 2022, EMBO Molecular Medicine.

Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function

Robin J. W. Willows, Parvathy E. Harikumar, Nathan R. Qi, 2016, Cell metabolism.

Chronic Activation of γ2 AMPK Induces Obesity and Reduces β Cell Function

Robin J. W. Willows, Parvathy E. Harikumar, Nathan R. Qi, 2016, Cell Metabolism.

Alpha-tropomyosin mutations in inherited cardiomyopathies

P. Robinson, C. Redwood, 2013, Journal of Muscle Research and Cell Motility.

Cardiac Excitation and Contraction Dilated cardiomyopathy mutations in thin-ﬁlament regulatory proteins reduce contractility, suppress systolic Ca 2 (cid:2) , and activate NFAT and Akt signaling

P. Robinson, C. Redwood, Suketu D Patel, 2020 .

Identification of Novel Interactions Between Domains of Myosin Binding Protein-C That Are Modulated by Hypertrophic Cardiomyopathy Missense Mutations

H. Watkins, J. Moolman-Smook, V. Corfield, 2002, Circulation research.

The reason for the low Ca2+-sensitivity of thin filaments associated with the Glu41Lys mutation in the TPM2 gene is "freezing" of tropomyosin near the outer domain of actin and inhibition of actin monomer switching off during the ATPase cycle.

C. Redwood, Y. Borovikov, S. V. Avrova, 2018, Biochemical and biophysical research communications.

Human DNA topoisomerases II alpha and II beta can functionally substitute for yeast TOP2 in chromosome segregation and recombination.

I. Hickson, J. Jenkins, C. Redwood, 1996, Molecular & general genetics : MGG.

Inhibition of actin-tropomyosin activation of myosin MgATPase activity by the smooth muscle regulatory protein caldesmon.

Steven B Marston, C. Redwood, 1992, The Journal of biological chemistry.

Novel Potential Treatment of Familial Hypertrophic Cardiomyopathy with Analogues of the Green Tea Polyphenol Epigallocatechin-3-Gallate

H. Watkins, B. Blagg, B. Casadei, 2016 .