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Publications

CalTrack: High Throughput Automated Calcium Transient Analysis in Cardiomyocytes.

Psaras Y. et al, (2021), Circ Res

Paracrine signalling by cardiac calcitonin controls atrial fibrogenesis and arrhythmia.

Moreira LM. et al, (2020), Nature

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+ & Activate NFAT & AKT Signalling

Robinson P. et al, (2020), American Journal of Physiology-Heart and Circulatory Physiology

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

Sparrow AJ. et al, (2020), American journal of physiology. Heart and circulatory physiology

Nitric Oxide and Mechano-Electrical Transduction in Cardiomyocytes.

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

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

Sparrow AJ. et al, (2019), Circulation Research

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

(2018), Journal of Biological Chemistry

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

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

Lakdawala NK. et al, (2010), J Am Coll Cardiol, 55, 320 - 329

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