[HTML][HTML] Loss of TMEM16A causes a defect in epithelial Ca2+-dependent chloride transport
J Ousingsawat, JR Martins, R Schreiber… - Journal of Biological …, 2009 - ASBMB
Molecular identification of the Ca 2+-dependent chloride channel TMEM16A (ANO1)
provided a fundamental step in understanding Ca 2+-dependent Cl− secretion in epithelia.
TMEM16A is an intrinsic constituent of Ca 2+-dependent Cl− channels in cultured epithelia
and may control salivary output, but its physiological role in native epithelial tissues remains
largely obscure. Here, we demonstrate that Cl− secretion in native epithelia activated by Ca
2+-dependent agonists is missing in mice lacking expression of TMEM16A. Ca 2+ …
provided a fundamental step in understanding Ca 2+-dependent Cl− secretion in epithelia.
TMEM16A is an intrinsic constituent of Ca 2+-dependent Cl− channels in cultured epithelia
and may control salivary output, but its physiological role in native epithelial tissues remains
largely obscure. Here, we demonstrate that Cl− secretion in native epithelia activated by Ca
2+-dependent agonists is missing in mice lacking expression of TMEM16A. Ca 2+ …