Area of research
Molecular Biology · Pulmonary and Respiratory Medicine
Research interest
Research interests include Cell biology, Chemistry, Cystic fibrosis transmembrane conductance regulator, Intracellular, Mucus, and Biology.
TMEM16A/F support exocytosis but do not inhibit Notch-mediated goblet cell metaplasia of BCi-NS1.1 human airway epithelium
Airway Delivery of Hydrogel-Encapsulated Niclosamide for the Treatment of Inflammatory Airway Disease
Paneth Cell Secretion in vivo Requires Expression of Tmem16a and Tmem16f
Mucus Release and Airway Constriction by TMEM16A May Worsen Pathology in Inflammatory Lung Disease
Gender-Dependent Phenotype in Polycystic Kidney Disease Is Determined by Differential Intracellular Ca2+ Signals
The chloride channel CFTR is not required for cyst growth in an ADPKD mouse model
Loss of PKD1 and PKD2 share common effects on intracellular Ca2+ signaling
Cyst growth in ADPKD is prevented by pharmacological and genetic inhibition of TMEM16A in vivo
Pharmacological Inhibition and Activation of the Ca2+ Activated Cl− Channel TMEM16A
Impaired Renal HCO3 - Excretion in Cystic Fibrosis
TMEM16A Mediates Mucus Production in Human Airway Epithelial Cells
TMEM16A drives renal cyst growth by augmenting Ca2+ signaling in M1 cells
TMEM16A deficiency: a potentially fatal neonatal disease resulting from impaired chloride currents
Niclosamide repurposed for the treatment of inflammatory airway disease
Contribution of Anoctamins to Cell Survival and Cell Death
TMEM16A in Cystic Fibrosis: Activating or Inhibiting?
Plasma membrane–localized TMEM16 proteins are indispensable for expression of CFTR
Control of Ion Transport by Tmem16a Expressed in Murine Intestine
TMEM16A is indispensable for basal mucus secretion in airways and intestine
Secretin-Stimulated Urinary HCO3- Excretion: A Function of CFTR and Pendrin
2018cited by 0position: middle
Differential effects of anoctamins on intracellular calcium signals
CFTR supports cell death through ROS-dependent activation of TMEM16F (anoctamin 6)
Acute Secretin-Induced Urinary HCO3- Excretion: A Function of Pendrin
2017cited by 0position: middle
Ca2+ signals, cell membrane disintegration, and activation of TMEM16F during necroptosis
Cellular defects by deletion of ANO10 are due to deregulated local calcium signaling
Non-essential contribution of LRRC8A to volume regulation
Relationship between TMEM16A/anoctamin 1 and LRRC8A
Modulating Ca2+ signals: a common theme for TMEM16, Ist2, and TMC