Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 594, Issue 1, Pages 19-30Publisher
WILEY
DOI: 10.1113/jphysiol.2014.275107
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Funding
- Wellcome Trust
- MRC
- National Science Foundation of China
- MRC [MR/K021303/1] Funding Source: UKRI
- Medical Research Council [MR/K021303/1, 1368213] Funding Source: researchfish
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Ca2+-activated chloride channels (CaCCs) regulate numerous physiological processes including epithelial transport, smooth muscle contraction and sensory processing. Anoctamin-1 (ANO1, TMEM16A) is a principal CaCC subunit in many cell types, yet our understanding of the mechanisms of ANO1 activation and regulation are only beginning to emerge. Ca2+ sensitivity of ANO1 is rather low and at negative membrane potentials the channel requires several micromoles of intracellular Ca2+ for activation. However, global Ca2+ levels in cells rarely reach such levels and, therefore, there must be mechanisms that focus intracellular Ca2+ transients towards the ANO1 channels. Recent findings indeed indicate that ANO1 channels often co-localize with sources of intracellular Ca2+ signals. Interestingly, it appears that in many cell types ANO1 is particularly tightly coupled to the Ca2+ release sites of the intracellular Ca2+ stores. Such preferential coupling may represent a general mechanism of ANO1 activation in native tissues.
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