Regulation of CFTR by AMPK

Description of projects available to graduate students:
We have characterized a novel interaction between the cystic fibrosis transmembrane conductance regulator (CFTR), the chloride channel that is defective in cystic fibrosis, and the AMP-activated protein kinase (AMPK), a cellular metabolic sensor which becomes active under conditions of metabolic stress. AMPK binds to, phosphorylates, and inhibits CFTR channel activity, predominantly by inhibiting channel gating. The underlying molecular mechanisms by which AMPK regulates CFTR are being explored.

Techniques graduate student will learn:
Two-electrode voltage clamp, patch-clamp electrophysiology, phosphorylation assays, transfection, viral transduction, DNA mutagenesis, RNA synthesis and expression in oocytes