A5021288289- Ion channel regulation and function
- Cardiac electrophysiology and arrhythmias
- Cardiomyopathy and Myosin Studies
- Fibroblast Growth Factor Research
- Neuroscience and Neural Engineering
- Neuroscience and Neuropharmacology Research
- Neurogenesis and neuroplasticity mechanisms
- Cardiovascular Effects of Exercise
- Erythrocyte Function and Pathophysiology
- Cardiac Arrhythmias and Treatments
- Electrochemical Analysis and Applications
- Receptor Mechanisms and Signaling
- Memory and Neural Mechanisms
- Advanced biosensing and bioanalysis techniques
Baylor College of Medicine
2024-2025
Washington University in St. Louis
2022-2023
Abstract Opening of the cardiac voltage-gated Na+ channel (Nav1.5) is responsible for robust depolarization action potential, while inactivation, which rapidly follows, allows repolarization. Regulation both voltage- and time-dependent kinetics Nav1.5 inactivation can alter ability heart to initiate sustain a re-entrant arrhythmia. The C-terminal domain (CTD) has been shown modulate fast channel, multiple auxiliary proteins bind CTD, including calmodulin (CaM) intracellular fibroblast growth...
Voltage-gated sodium (NaV) channels are responsible for the initiation and propagation of action potentials. In heart, predominant NaV1.5 α subunit is composed four homologous repeats (I–IV) forms a macromolecular complex with multiple accessory proteins, including intracellular fibroblast growth factors (iFGF). spite high homology, each iFGFs, iFGF11–iFGF14, as well individual iFGF splice variants, differentially regulates NaV channel gating, mechanisms underlying these differential effects...
Abstract BK type Ca 2+ -activated K + channels activate in response to both voltage and . The membrane-spanning sensor domain (VSD) activation binding the cytosolic tail (CTD) open pore across membrane, but mechanisms that couple VSD opening are not clear. Here we show a compound, BC5, identified from silico screening, interacts with CTD-VSD interface specifically modulates dependent mechanism. BC5 activates channel absence of inhibits effects. Thus, perturbs pathway couples allosterically...
Missense variants in calmodulin (CaM) predispose patients to arrhythmias associated with high mortality rates. As CaM regulates several key cardiac ion channels, a mechanistic understanding of variant-associated requires elucidating individual variant effect on distinct channels. One regulatory target is the KCNQ1 (K V 7.1) voltage-gated potassium channel that underlie I Ks current. Yet, relatively little known as how interact or affect its function.To observe arrhythmia-associated binding...
Excitatory synapses and the actin-rich dendritic spines on which they reside are indispensable for information processing storage in brain. In adult hippocampus, excitatory must balance plasticity stability to support learning memory. However, mechanisms governing this remain poorly understood. Tiam1 is an actin cytoskeleton regulator prominently expressed dentate gyrus (DG) throughout life. Previously, we showed that promotes granule cell synapse spine stabilization during development, but...
Missense variants in calmodulin (CaM) predispose patients to arrhythmias associated with high mortality rates ("calmodulinopathy"). As CaM regulates many key cardiac ion channels, an understanding of disease mechanism variant requires elucidating individual effects on distinct channels. One regulatory target is the KCNQ1 (KV7.1) voltage-gated potassium channel that carries IKs current. Yet, relatively little known as how interact or affect its function. Here, we take a multipronged approach...
Abstract BK type Ca 2+ -activated K + channels activate in response to both the membrane voltage and intracellular with distinct mechanisms. binds cytosolic domain (CTD) open pore across membrane, but mechanism that couples binding opening is not clear. Here we show a compound, BC5, identified using silico screening, interacts at interface between CTD transmembrane sensing (VSD) enhances channel activity by specifically affecting dependent mechanism. BC5 activates absence of inhibits...