Author
Listed:
- Young Duk Yang
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Hawon Cho
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Jae Yeon Koo
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Min Ho Tak
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Yeongyo Cho
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Won-Sik Shim
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Seung Pyo Park
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Jesun Lee
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Byeongjun Lee
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Byung-Moon Kim
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Ramin Raouf
(Molecular Nociception Group, Neuroscience, Physiology and Pharmacology, University College London)
- Young Ki Shin
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
- Uhtaek Oh
(Sensory Research Center, CRI, College of Pharmacy, Seoul National University)
Abstract
Calcium (Ca2+)-activated chloride channels are fundamental mediators in numerous physiological processes including transepithelial secretion, cardiac and neuronal excitation, sensory transduction, smooth muscle contraction and fertilization. Despite their physiological importance, their molecular identity has remained largely unknown. Here we show that transmembrane protein 16A (TMEM16A, which we also call anoctamin 1 (ANO1)) is a bona fide Ca2+-activated chloride channel that is activated by intracellular Ca2+ and Ca2+-mobilizing stimuli. With eight putative transmembrane domains and no apparent similarity to previously characterized channels, ANO1 defines a new family of ionic channels. The biophysical properties as well as the pharmacological profile of ANO1 are in full agreement with native Ca2+-activated chloride currents. ANO1 is expressed in various secretory epithelia, the retina and sensory neurons. Furthermore, knockdown of mouse Ano1 markedly reduced native Ca2+-activated chloride currents as well as saliva production in mice. We conclude that ANO1 is a candidate Ca2+-activated chloride channel that mediates receptor-activated chloride currents in diverse physiological processes.
Suggested Citation
Young Duk Yang & Hawon Cho & Jae Yeon Koo & Min Ho Tak & Yeongyo Cho & Won-Sik Shim & Seung Pyo Park & Jesun Lee & Byeongjun Lee & Byung-Moon Kim & Ramin Raouf & Young Ki Shin & Uhtaek Oh, 2008.
"TMEM16A confers receptor-activated calcium-dependent chloride conductance,"
Nature, Nature, vol. 455(7217), pages 1210-1215, October.
Handle:
RePEc:nat:nature:v:455:y:2008:i:7217:d:10.1038_nature07313
DOI: 10.1038/nature07313
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Cited by:
- Melanie Arndt & Carolina Alvadia & Monique S. Straub & Vanessa Clerico Mosina & Cristina Paulino & Raimund Dutzler, 2022.
"Structural basis for the activation of the lipid scramblase TMEM16F,"
Nature Communications, Nature, vol. 13(1), pages 1-17, December.
- Weijia Sun & Shuai Guo & Yuheng Li & JianWei Li & Caizhi Liu & Yafei Chen & Xuzhao Wang & Yingjun Tan & Hua Tian & Cheng Wang & Ruikai Du & Guohui Zhong & Sai Shi & Biao Ma & Chang Qu & Jingxuan Fu & , 2022.
"Anoctamin 1 controls bone resorption by coupling Cl− channel activation with RANKL-RANK signaling transduction,"
Nature Communications, Nature, vol. 13(1), pages 1-15, December.
- Andy K. M. Lam & Sonja Rutz & Raimund Dutzler, 2022.
"Inhibition mechanism of the chloride channel TMEM16A by the pore blocker 1PBC,"
Nature Communications, Nature, vol. 13(1), pages 1-13, December.
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