NDLI: Relationship between TMEM16A/anoctamin 1 and LRRC8A

Content Provider	Springer Nature Link
Author	Benedetto, Roberta Sirianant, Lalida Pankonien, Ines Wanitchakool, Podchanart Ousingsawat, Jiraporn Cabrita, Ines Schreiber, Rainer Amaral, Margarida Kunzelmann, Karl
Copyright Year	2016
Abstract	TMEM16A/anoctamin 1/ANO1 and VRAC/LRRC8 are independent chloride channels activated either by increase in intracellular Ca2+ or cell swelling, respectively. In previous studies, we observed overlapping properties for both types of channels. (i) TMEM16A/ANO1 and LRRC8 are inhibited by identical compounds, (ii) the volume-regulated anion channel VRAC requires compartmentalized Ca2+ increase to be fully activated, (iii) anoctamins are activated by cell swelling, (iv) both channels have a role for apoptotic cell death, (v) both channels are possibly located in lipid rafts/caveolae like structures, and (vi) VRAC and anoctamin 1 currents are not additive when each are fully activated. In the present study, we demonstrate in different cell types that loss of LRRC8A expression not only inhibited VRAC, but also attenuated Ca2+ activated Cl− currents. Moreover, expression of LRRC8A enhanced Ca2+ activated Cl− currents, and both LRRC8A and ANO1 could be coimmunoprecipitated. We found that LRRC8A becomes accessible to biotinylation upon exposure to hypotonic bath solution, while membrane capacitance was not enhanced. When intracellular Ca2+ was increased in ANO1-expressing cells, the membrane capacitance was enhanced and increased binding of FM4–64 to the membrane was observed. As this was not seen in cells lacking ANO1 expression, a role of ANO1 for exocytosis was suggested. We propose that ANO1 and LRRC8A are activated in parallel. Thus, ionomycin or purinergic stimulation will not only activate ANO1 but also LRRC8 currents. Cell swelling will not only activate LRRC8/VRAC, but also stimulate ANO1 currents by enhancing compartmentalized Ca2+ increase and/or through swelling induced autocrine release of ATP.
Starting Page	1751
Ending Page	1763
Page Count	13
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	468
Issue Number	10
e-ISSN	14322013
Language	English
Publisher	Springer Berlin Heidelberg
Publisher Date	2016-08-12
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	LRRC8A VRAC Volume-activated anion channels Ca2+-activated chloride currents TMEM16A Anoctamin 1 Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Relationship between TMEM16A/anoctamin 1 and LRRC8A

Non-essential contribution of LRRC8A to volume regulation

Cl− channels in apoptosis

Cellular volume regulation by anoctamin 6: Ca2+, phospholipase A2 and osmosensing

Anoctamins support calcium-dependent chloride secretion by facilitating calcium signaling in adult mouse intestine

Expression of anoctamins in retinal pigment epithelium (RPE)

Interaction between TRP and $Ca^{2+}$-activated chloride channels

Biophysics and Physiology of the Volume-Regulated Anion Channel (VRAC)/Volume-Sensitive Outwardly Rectifying Anion Channel (VSOR)

ER-localized bestrophin 1 activates Ca2+-dependent ion channels TMEM16A and SK4 possibly by acting as a counterion channel

Relationship between TMEM16A/anoctamin 1 and LRRC8A

Similar Documents

Relationship between TMEM16A/anoctamin 1 and LRRC8A

Non-essential contribution of LRRC8A to volume regulation

Cl− channels in apoptosis

Cellular volume regulation by anoctamin 6: Ca2+, phospholipase A2 and osmosensing

Anoctamins support calcium-dependent chloride secretion by facilitating calcium signaling in adult mouse intestine

Expression of anoctamins in retinal pigment epithelium (RPE)

Interaction between TRP and $Ca^{2+}$-activated chloride channels

Biophysics and Physiology of the Volume-Regulated Anion Channel (VRAC)/Volume-Sensitive Outwardly Rectifying Anion Channel (VSOR)

ER-localized bestrophin 1 activates Ca2+-dependent ion channels TMEM16A and SK4 possibly by acting as a counterion channel

Relationship between TMEM16A/anoctamin 1 and LRRC8A