Area of research
Molecular Biology · Pulmonary and Respiratory Medicine
Research interest
Research interests include Cystic fibrosis transmembrane conductance regulator, Epithelial sodium channel, Cystic fibrosis, Medicine, Lung, and Chemistry.
Oxidative damage to lung mitochondrial DNA is a key contributor to the development of chemical lung injury
Low molecular weight hyaluronan inhibits lung epithelial ion channels by activating the calcium-sensing receptor
Hypoxia‐induced cystic fibrosis transmembrane conductance regulator dysfunction is a universal mechanism underlying reduced mucociliary transport in sinusitis
Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems
LPS decreases CFTR open probability and mucociliary transport through generation of reactive oxygen species
Reactive species generated by heme impair alveolar epithelial sodium channel function in acute respiratory distress syndrome
Upregulation of airway smooth muscle calcium-sensing receptor by low-molecular-weight hyaluronan
Influenza-mediated reduction of lung epithelial ion channel activity leads to dysregulated pulmonary fluid homeostasis
Resveratrol and ivacaftor are additive G551D CFTR‐channel potentiators: therapeutic implications for cystic fibrosis sinus disease
Influenza virus infection alters ion channel function of airway and alveolar cells: mechanisms and physiological sequelae
Hyaluronan mediates airway hyperresponsiveness in oxidative lung injury
Influenza virus M2 targets cystic fibrosis transmembrane conductance regulator for lysosomal degradation during viral infection
Chlorine inhalation-induced myocardial depression and failure
A synonymous codon change alters the drug sensitivity of ΔF508 cystic fibrosis transmembrane conductance regulator
Sinupret Activates CFTR and TMEM16A-Dependent Transepithelial Chloride Transport and Improves Indicators of Mucociliary Clearance
A Novel Tumor Necrosis Factor–mediated Mechanism of Direct Epithelial Sodium Channel Activation
The silent codon change I507‐ATC→ATT contributes to the severity of the ΔF508 CFTR channel dysfunction
Influenza matrix protein 2 alters CFTR expression and function through its ion channel activity
Inter-α-Inhibitor Blocks Epithelial Sodium Channel Activation and Decreases Nasal Potential Differences in ΔF508 Mice
The CFTR and ENaC debate: how important is ENaC in CF lung disease?