Associated Papers
Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human β-cardiac myosin allosterically.
Nandwani N et al.
Nature Communications, 2025
Reassessing the unifying hypothesis for hypercontractility caused by myosin mutations in hypertrophic cardiomyopathy.
Spudich JA et al.
The Embo Journal, 2024
YAP dysregulation triggers hypertrophy by CCN2 secretion and TGFβ uptake in human pluripotent stem cell-derived cardiomyocytes.
Chirikian O et al.
Biorxiv : the Preprint Server for Biology, 2024
Incomplete-penetrant hypertrophic cardiomyopathy MYH7 G256E mutation causes hypercontractility and elevated mitochondrial respiration.
Lee S et al.
Proceedings of the National Academy of Sciences of the United States of America, 2024
Multinational experience with next-generation sequencing: opportunity to identify transthyretin cardiac amyloidosis and Fabry disease.
Silva SME et al.
Cardiovascular Diagnosis and Therapy, 2024
Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human beta-cardiac myosin allosterically.
Nandwani N et al.
Biorxiv : the Preprint Server for Biology, 2024
Assessing Cardiac Contractility From Single Molecules to Whole Hearts.
Garg A et al.
Jacc. Basic to Translational Science, 2024
Homologous mutations in human β, embryonic, and perinatal muscle myosins have divergent effects on molecular power generation.
Liu C et al.
Proceedings of the National Academy of Sciences of the United States of America, 2024
MYH7 in cardiomyopathy and skeletal muscle myopathy.
Gao Y et al.
Molecular and Cellular Biochemistry, 2024
Homologous mutations in β, embryonic, and perinatal muscle myosins have divergent effects on molecular power generation.
Liu C et al.
Biorxiv : the Preprint Server for Biology, 2023
Multi-scale models reveal hypertrophic cardiomyopathy MYH7 G256E mutation drives hypercontractility and elevated mitochondrial respiration.
Lee S et al.
Biorxiv : the Preprint Server for Biology, 2023
Cryo-EM structure of the folded-back state of human β-cardiac myosin.
Grinzato A et al.
Biorxiv : the Preprint Server for Biology, 2023
Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy.
Ušaj M et al.
International Journal of Molecular Sciences, 2022
Hypertrophic cardiomyopathy: Mutations to mechanisms to therapies.
Kawana M et al.
Frontiers in Physiology, 2022
The hypertrophic cardiomyopathy mutations R403Q and R663H increase the number of myosin heads available to interact with actin.
Sarkar SS et al.
Science Advances, 2020
The mesa trail and the interacting heads motif of myosin II.
Woodhead JL et al.
Archives of Biochemistry and Biophysics, 2020
Direct Sarcomere Modulators Are Promising New Treatments for Cardiomyopathies.
Tsukamoto O
International Journal of Molecular Sciences, 2019
Myosin motor domains carrying mutations implicated in early or late onset hypertrophic cardiomyopathy have similar properties.
Vera CD et al.
The Journal of Biological Chemistry, 2019
β-Cardiac myosin hypertrophic cardiomyopathy mutations release sequestered heads and increase enzymatic activity.
Adhikari AS et al.
Nature Communications, 2019
SETD3 is an actin histidine methyltransferase that prevents primary dystocia.
Wilkinson AW et al.
Nature, 2019
Deciphering the super relaxed state of human β-cardiac myosin and the mode of action of mavacamten from myosin molecules to muscle fibers.
Anderson RL et al.
Proceedings of the National Academy of Sciences of the United States of America, 2018
Controlling load-dependent kinetics of β-cardiac myosin at the single-molecule level.
Liu C et al.
Nature Structural & Molecular Biology, 2018
The myosin mesa and the basis of hypercontractility caused by hypertrophic cardiomyopathy mutations.
Nag S et al.
Nature Structural & Molecular Biology, 2017
Biophysical properties of human β-cardiac myosin with converter mutations that cause hypertrophic cardiomyopathy.
Kawana M et al.
Science Advances, 2017
Early-Onset Hypertrophic Cardiomyopathy Mutations Significantly Increase the Velocity, Force, and Actin-Activated ATPase Activity of Human β-Cardiac Myosin.
Adhikari AS et al.
Cell Reports, 2016