Area of research
Cardiology and Cardiovascular Medicine · Molecular Biology
Research interest
Research interests include Cardiac electrophysiology and arrhythmias, Ion channel regulation and function, Cardiomyopathy and Myosin Studies, and Neuroscience and Neuropharmacology Research.
HCN4 channels sense temperature and determine heart rate responses to heat.
An improved reporter identifies ruxolitinib as a potent and cardioprotective CaMKII inhibitor
An improved reporter identifies ruxolitinib as a potent and cardioprotective CaMKII inhibitor.
Genome-wide CRISPR screen reveals genetic modifiers of Ca
<sup>2+</sup>
-mediated cell death
CaMKII as a Therapeutic Target in Cardiovascular Disease
Heart Failure and Atrial Fibrillation-Chicken or Egg?
Excessive <i>O</i> -GlcNAcylation Causes Heart Failure and Sudden Death
Excessive
<i>O</i>
-GlcNAcylation Causes Heart Failure and Sudden Death
CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.
PDE1 Inhibition Modulates Ca<sub>v</sub>1.2 Channel to Stimulate Cardiomyocyte Contraction.
Loss of CASK Accelerates Heart Failure Development.
Totally Rad? The Long and Winding Road to Understanding Ca
<sub>V</sub>
1.2 Regulation
Voices for Social Justice and Against Racism: An AAIM Perspective
Boost US federal funding for international trainees.
Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy
Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy.
MICAL1 constrains cardiac stress responses and protects against disease by oxidizing CaMKII
PDE1 inhibition modulates Ca<sub>v</sub>1.2 channel to stimulate cardiomyocyte contraction
Chronic Calmodulin-Kinase II Activation Drives Disease Progression in Mutation-Specific Hypertrophic Cardiomyopathy
E-C coupling structural protein junctophilin-2 encodes a stress-adaptive transcription regulator
Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart
The mitochondrial uniporter controls fight or flight heart rate increases
Microtubule-Mediated Defects in Junctophilin-2 Trafficking Contribute to Myocyte Transverse-Tubule Remodeling and Ca <sup>2+</sup> Handling Dysfunction in Heart Failure
Progress toward the prevention and treatment of atrial fibrillation: A summary of the Heart Rhythm Society Research Forum on the Treatment and Prevention of Atrial Fibrillation, Washington, DC, December 9–10, 2013
Oxidized Ca <sup>2+</sup> /Calmodulin-Dependent Protein Kinase II Triggers Atrial Fibrillation
Ionizing radiation regulates cardiac Ca handling via increased ROS and activated CaMKII
Phosphoproteomics Study Based on In Vivo Inhibition Reveals Sites of Calmodulin‐Dependent Protein Kinase II Regulation in the Heart
CaMKII effects on inotropic but not lusitropic force frequency responses require phospholamban