Expression and Function of Epithelial Anoctamins

Schreiber, Rainer and Uliyakina, Inna and Kongsuphol, Patthara and Warth, Richard and Mirza, Myriam and Martins, Joana R. and Kunzelmann, Karl (2010) Expression and Function of Epithelial Anoctamins. JOURNAL OF BIOLOGICAL CHEMISTRY, 285 (10). pp. 7838-7845. ISSN 0021-9258, 1083-351X

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Abstract

The calcium-activated chloride channel anoctamin1 (ANO1; TMEM16A) is fundamental for the function of epithelial organs. Mice lacking ANO1 expression exhibit transport defects and a pathology similar to cystic fibrosis. They also show a general defect of epithelial electrolyte transport. Here we analyzed expression of all ten members (ANO1-ANO10) in a broad range of murine tissues and detected predominant expression of ANO1, 6, 7, 8, 9, 10 in epithelial tissues, while ANO2, 3, 4, 5 are common in neuronal and muscle tissues. When expressed in Fisher Rat Thyroid (FTR) cells, all ANO proteins localized to the plasma membrane but only ANO1, 2, 6, and 7 produced Ca2+ activated Cl- conductance, as analyzed by ATP-induced iodide quenching of YFP fluorescence. In contrast ANO9 and ANO10 suppressed baseline Cl- conductance and coexpression of ANO9 with ANO1 inhibited ANO1 activity. Patch clamping of ANO-expressing FRT cells indicated that apart from ANO1 also ANO6 and 10 produced chloride currents, albeit with very different Ca2+ sensitivity and activation time. We conclude that each tissue expresses a set of anoctamins that form cell- and tissue-specific Ca2+-dependent Cl- channels.

Item Type: Article
Uncontrolled Keywords: ACTIVATED CHLORIDE CHANNELS; ION-TRANSPORT; PROTEIN; CELLS; TMEM16A; BESTROPHIN; COMPLEX; CANCER;
Subjects: 500 Science > 570 Life sciences
Divisions: Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Karl Kunzelmann
Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Richard Warth
Depositing User: Dr. Gernot Deinzer
Date Deposited: 03 Aug 2020 11:27
Last Modified: 03 Aug 2020 11:27
URI: https://pred.uni-regensburg.de/id/eprint/24985

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