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

CalTrack: High-Throughput Automated Calcium Transient Analysis in Cardiomyocytes.

Psaras Y. et al, (2021), Circ Res, 129, 326 - 341

Paracrine signalling by cardiac calcitonin controls atrial fibrogenesis and arrhythmia.

Moreira LM. et al, (2020), Nature, 587, 460 - 465

Calcitonin paracrine signaling controls atrial fibrogenesis and arrhythmia

MOREIRA LM. et al, (2020), Nature

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

Robinson P. et al, (2020), Am J Physiol Heart Circ Physiol, 319, H306 - H319

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

Nitric Oxide and Mechano-Electrical Transduction in Cardiomyocytes.

Boycott HE. et al, (2020), Front Physiol, 11

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

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

Fluorescent, Bioluminescent, and Optogenetic Approaches to Study Excitable Physiology in the Single Cardiomyocyte.

Broyles CN. et al, (2018), Cells, 7

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

Robinson PJ. et al, (2016), BIOPHYSICAL JOURNAL, 110, 125A - 125A

P123The rescue of Ca2+ cycling abnormalities conferred by HCM-causing mutations with analogues of the green tea polyphenol epigallocatechin-3-gallate.

Robinson P. et al, (2014), Cardiovasc Res, 103 Suppl 1

P387Knock-in mouse model of PRKAG2 cardiomyopathy (R299Q) exhibits altered Ca2+-dependent cardiac contractility and reduced protein kinase A activity.

Turtle C. et al, (2014), Cardiovasc Res, 103 Suppl 1

Alpha-tropomyosin mutations in inherited cardiomyopathies.

Redwood C. and Robinson P., (2013), J Muscle Res Cell Motil, 34, 285 - 294

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

Karpicheva OE. et al, (2013), Arch Biochem Biophys, 536, 25 - 30

Cardiomyopathy-Causing Mutations in Thin Filament Regulatory Proteins Acutely Affeect Ca2+-Buffering and Ca2+-Dependent Signalling In Situ

Robinson P. et al, (2013), BIOPHYSICAL JOURNAL, 104, 362A - 362A

Cardiomyopathy-causing mutations in cardiac thin filament regulatory proteins acutely affect Ca2+ buffering and Ca2+ dependant signalling in situ

Robinson P. et al, (2012), CARDIOVASCULAR RESEARCH, 93, S50 - S51

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

Borovikov YS. et al, (2011), Biochem Biophys Res Commun, 411, 496 - 500

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

Borovikov YS. et al, (2011), Biochemical and Biophysical Research Communications, 411, 496 - 500

Functional investigation of beta-tropomyosin mutations that cause congenital skeletal myopathies

Piers A. et al, (2011), NEUROMUSCULAR DISORDERS, 21, S25 - S26

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