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Search results (50)

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Selective blockade of microRNA-31-5p/calcitonin receptor interaction reverses established atrial fibrosis and atrial arrhythmia substrate.

Trompf J. et al, (2026), Res Sq

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

Nitric Oxide and Mechano-Electrical Transduction in Cardiomyocytes

BOYCOTT HE. et al, (2021), Frontiers in Physiology, 11

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

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