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The Journal of Biological Chemistry|February 12, 2004
The primary substrate binding site in the b' domain of ERp57 is adapted for endoplasmic reticulum lectin associationSarah J Russell, Lloyd W Ruddock, Kirsi E H Salo, et al.
Life Science Alliance|September 20, 2024
PRDM16 determines specification of ventricular cardiomyocytes by suppressing alternative cell fatesJore Van Wauwe, Alexia Mahy, Sander Craps, et al.
Journal of Molecular and Cellular Cardiology|December 24, 2017
Calcium phosphate particles stimulate interleukin-1β release from human vascular smooth muscle cells: A role for spleen tyrosine kinase and exosome releaseYana Dautova, Alexander N Kapustin, Kevin Pappert, et al.
Cardiovascular Research|April 19, 2018
Hyperactive ryanodine receptors in human heart failure and ischaemic cardiomyopathy reside outside of couplonsEef Dries, Demetrio J Santiago, Guillaume Gilbert, et al.
Journal of Cell Science|August 26, 2016
Exosomes bind to autotaxin and act as a physiological delivery mechanism to stimulate LPA receptor signalling in cellsSusanna A Jethwa, Emma J Leah, Qifeng Zhang, et al.
Briefings in Bioinformatics|July 24, 2025
Benchmarking of computational demultiplexing methods for single-nucleus RNA sequencing dataYile Fu, Mohamad Youness, Alessia Virzì, et al.
Biochemical Pharmacology|March 22, 2017
Basal ryanodine receptor activity suppresses autophagic fluxTim Vervliet, Isabel Pintelon, Kirsten Welkenhuyzen, et al.
Proceedings of the National Academy of Sciences of the United States of America|January 8, 2014
Feedback regulation mediated by Bcl-2 and DARPP-32 regulates inositol 1,4,5-trisphosphate receptor phosphorylation and promotes cell survivalMing-Jin Chang, Fei Zhong, Andrew R Lavik, et al.
Journal of Molecular and Cellular Cardiology|April 1, 2023
InsP<sub>3</sub>R-RyR channel crosstalk augments sarcoplasmic reticulum Ca<sup>2+</sup> release and arrhythmogenic activity in post-MI pig cardiomyocytesXin Jin, Anna Meletiou, Joshua Chung, et al.
The Journal of Physiology|January 5, 2020
Altered adrenergic response in myocytes bordering a chronic myocardial infarction underlies in vivo triggered activity and repolarization instabilityEef Dries, Matthew Amoni, Bert Vandenberk, et al.
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