Area of research
Molecular Biology · Physiology
Research interest
Research interests include Ion channel regulation and function, Pain Mechanisms and Treatments, Neuroscience and Neuropharmacology Research, and Cardiac electrophysiology and arrhythmias.
VTA dopaminergic neurons involved in chronic spared nerve injury pain-induced depressive-like behavior
Depression-related innate immune genes and pan-cancer gene analysis and validation
Discovery of E0199: A novel compound targeting both peripheral NaV and KV7 channels to alleviate neuropathic pain
Therapeutic Targeting of Potassium Channels
Three sesquiterpene lactones suppress lung adenocarcinoma by blocking TMEM16A-mediated Ca<sup>2+</sup>-activated Cl<sup>−</sup> channels
The Role of VTA Dopaminergic Neurons in Chronic Peripheral Neuropathic Pain- induced Depressive-like Behavior
Activation of parabrachial nucleus - ventral tegmental area pathway underlies the comorbid depression in chronic neuropathic pain in mice
Junctophilin‐4 facilitates inflammatory signalling at plasma membrane‐endoplasmic reticulum junctions in sensory neurons
Delineating an extracellular redox-sensitive module in T-type Ca2+ channels
Volume-regulated Cl<sup>−</sup> current: contributions of distinct Cl<sup>−</sup> channels and localized Ca<sup>2+</sup> signals
Junctophilin-4 is essential for signalling at plasma membrane-endoplasmic reticulum junctions in sensory neurons
Modulation of KCNQ Channels by Intracellular Zinc
Intracellular zinc activates KCNQ channels by reducing their dependence on phosphatidylinositol 4,5-bisphosphate
Inflammatory mediator bradykinin increases population of sensory neurons expressing functional T-type Ca2+ channels
Suppression of KV7/KCNQ potassium channel enhances neuronal differentiation of PC12 cells
GABAB receptors inhibit low-voltage activated and high-voltage activated Ca2+ channels in sensory neurons via distinct mechanisms
Inhibition of T-type Ca2+ Channels by Hydrogen Sulfide
Control of somatic membrane potential in nociceptive neurons and its implications for peripheral nociceptive transmission
Characterization of the effects of Cl− channel modulators on TMEM16A and bestrophin-1 Ca2+ activated Cl− channels
Hydrogen sulfide inhibits Cav3.2 T‐type Ca <sup>2+</sup> channels
P64 Hydrogen sulfide inhibits Cav 3.2 T-type Ca2+ channels
Ion Channels Controlling Resting Membrane Potential of Nociceptive DRG Neuron Somata
The Role of Potassium Channel Activation in Celecoxib-Induced Analgesic Action
Agonist-Dependent Potentiation of Vanilloid Receptor Transient Receptor Potential Vanilloid Type 1 Function by Stilbene Derivatives