Area of research
Surgery · Oncology
Research interest
Research focused on Calcineurin and Acinar cell, with related work in Pancreatitis, NFAT, Exocytosis. Notable publications include 'Bile Acids Induce Pancreatic Acinar Cell Injury and Pancreatitis by Activating Calcineurin', 'Pancreatitis-Induced Depletion of Syntaxin 2 Promotes Autophagy and Increases Basolateral Exocytosis', and 'Exposure to Radiocontrast Agents Induces Pancreatic Inflammation by Activation of Nuclear Factor-κB, Calcium Signaling, and Calcineurin'.
Pancreatitis is an FGF21-deficient state that is corrected by replacement therapy
The Protective Effects of Calcineurin on Pancreatitis in Mice Depend on the Cellular Source
Pancreatitis-Induced Depletion of Syntaxin 2 Promotes Autophagy and Increases Basolateral Exocytosis
Exposure to Radiocontrast Agents Induces Pancreatic Inflammation by Activation of Nuclear Factor-κB, Calcium Signaling, and Calcineurin
Cluster of Differentiation 38 (CD38) Mediates Bile Acid-induced Acinar Cell Injury and Pancreatitis through Cyclic ADP-ribose and Intracellular Calcium Release
Bile Acids Induce Pancreatic Acinar Cell Injury and Pancreatitis by Activating Calcineurin
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