Publications — Radcliffe Department of Medicine

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

Robinson P. et al, (2023), J Mol Cell Cardiol, 180, 44 - 57

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

Toepfer CN. et al, (2020), Circulation, 141, 828 - 842

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

Sparrow AJ. et al, (2020), Am J Physiol Heart Circ Physiol, 318, H715 - H722

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

Borovikov YS. et al, (2020), Biochem Biophys Res Commun, 523, 258 - 262

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

Prondzynski M. et al, (2019), EMBO Mol Med, 11

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

Avrova SV. et al, (2019), Biochem Biophys Res Commun

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

Sparrow AJ. et al, (2019), Circ Res, 124, 1228 - 1239

Hypertrophic cardiomyopathy mutations in MYBPC3 dysregulate myosin.

Toepfer CN. et al, (2019), Sci Transl Med, 11

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

Piroddi N. et al, (2019), J Gen Physiol, 151, 18 - 29

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

Kresin N. et al, (2019), Front Physiol, 10

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.

Borovikov YS. et al, (2018), Int J Mol Sci, 19

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

Toepfer CN. et al, (2018), CIRCULATION RESEARCH, 123

Mutant Muscle LIM Protein C58G causes cardiomyopathy through protein depletion.

Ehsan M. et al, (2018), J Mol Cell Cardiol, 121, 287 - 296

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.

Avrova SV. et al, (2018), Biochem Biophys Res Commun, 502, 209 - 214

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

Robinson P. et al, (2018), J Biol Chem, 293, 10487 - 10499

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

Rysev NA. et al, (2018), Cell and Tissue Biology, 12, 238 - 246

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.

Borovikov YS. et al, (2017), Biochem Biophys Res Commun, 494, 681 - 686

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

Borovikov YS. et al, (2017), Sci Rep, 7

Mammalian γ2 AMPK regulates intrinsic heart rate.

Yavari A. et al, (2017), Nat Commun, 8

Activation of Autophagy Ameliorates Cardiomyopathy in Mybpc3-Targeted Knockin Mice.

Singh SR. et al, (2017), Circ Heart Fail, 10

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