ArticlePflugers Archiv : European journal of physiology2013
Acid-sensitive outwardly rectifying (ASOR) anion channels in human epithelial cells are highly sensitive to temperature and independent of ClC-3.
Article in Pflugers Archiv : European journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27 citing papers in PubMed, 40 citations in OpenAlex.
- Conformational Fingerprints Underlying Thermal Modulation of PAC/TMEM206 Gating.International journal of molecular sciences · 2026Article
- Article
- Article
- Functional expression of the proton sensors ASIC1a, TMEM206, and OGR1 together with BKPflugers Archiv : European journal of physiology · 2024Article
- Physiological Functions of the Volume-Regulated Anion Channel VRAC/LRRC8 and the Proton-Activated Chloride Channel ASOR/TMEM206.Handbook of experimental pharmacology · 2024Article
- CBA (4-chloro-2-(2-chlorophenoxy)acetamido) benzoic acid) inhibits TMEM206 mediated currents and TMEM206 does not contribute to acid-induced cell death in colorectal cancer cells.Frontiers in pharmacology · 2024Article
- A new polymodal gating model of the proton-activated chloride channel.PLoS biology · 2023Article
- Review
- Molecular mechanism underlying desensitization of the proton-activated chloride channel PAC.eLife · 2022Article
- Molecular determinants of pH sensing in the proton-activated chloride channel.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- pH and proton-sensitive receptors in brain ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Proton-gated anion transport governs macropinosome shrinkage.Nature cell biology · 2022Article
- Cryo-EM structure of a proton-activated chloride channel TMEM206.Science advances · 2021Article
- Proton-activated chloride channel PAC regulates endosomal acidification and transferrin receptor-mediated endocytosis.Cell reports · 2021Article
- Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 2: Functional and Molecular Properties of ASOR/PAC Channels and Their Roles in Cell Volume Dysregulation and Acidotoxic Cell Death.Frontiers in cell and developmental biology · 2021Review
- From Pinocytosis to Methuosis-Fluid Consumption as a Risk Factor for Cell Death.Frontiers in cell and developmental biology · 2021Review
- PAC proton-activated chloride channel contributes to acid-induced cell death in primary rat cortical neurons.Channels (Austin, Tex.) · 2020Article
- Acid- and Volume-Sensitive Chloride Currents in Human Chondrocytes.Frontiers in cell and developmental biology · 2020Article
- Identification of TMEM206 proteins as pore of PAORAC/ASOR acid-sensitive chloride channels.eLife · 2019Article
- Acid- and Volume-Sensitive Chloride Currents in Microglial Cells.International journal of molecular sciences · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A novel type of anion channel activated by extracellular acidification, called acid-sensitive outwardly rectifying (ASOR) anion channel, was shown to be involved in acidotoxic necrotic death in human epithelial cells. However, its biophysical property and molecular identity have remained elusive. In human epithelial HeLa cells, here, whole-cell currents of ASOR anion channel were found to be augmented by warm temperature, with a threshold temperature of 32 °C. Temperature sensitivity of the conductance was found to be high (with Q 10 of 8.8) in the range of body temperature, suggesting a possible involvement of a non-diffusion-limited process such as a transporter-mediated conduction. In this regard, it is interesting that a Cl(-)/H(+) antiporter ClC-3 has recently been proposed as a candidate for the ASOR channel. However, siRNA-mediated knockdown of hClC-3 failed to suppress ASOR currents in HeLa cells. Also, endogenous ASOR currents in HEK293T cells were not affected by overexpression of human or mouse ClC-3. Furthermore, functional expression of the ASOR channel was virtually absent in the cisplatin-resistant human cancer KCP-4 cell line despite the fact that molecular expression of ClC-3 was indistinguishable between KCP-4 cells and parental cisplatin-sensitive KB-3-1 cells which endogenously exhibit high activity of ASOR anion channels. These results indicate that the ASOR anion channel is highly sensitive to temperature and independent of ClC-3.
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