ArticleChannels (Austin, Tex.)2014
Temperature sensitivity of acid-sensitive outwardly rectifying (ASOR) anion channels in cortical neurons is involved in hypothermic neuroprotection against acidotoxic necrosis.
Article in Channels (Austin, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Conformational Fingerprints Underlying Thermal Modulation of PAC/TMEM206 Gating.International journal of molecular sciences · 2026Article
- Article
- 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
- 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
- Gating choreography and mechanism of the human proton-activated chloride channel ASOR.Science advances · 2022Article
- Ion permeation controlled by hydrophobic residues and proton binding in the proton-activated chloride channel.iScience · 2021Article
- Cryo-EM structure of a proton-activated chloride channel TMEM206.Science advances · 2021Article
- Low pH Attenuates Apoptosis by Suppressing the Volume-Sensitive Outwardly Rectifying (VSOR) Chloride Current in Chondrocytes.Frontiers in cell and developmental biology · 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
- Properties, Structures, and Physiological Roles of Three Types of Anion Channels Molecularly Identified in the 2010's.Frontiers in physiology · 2021Review
- PAC proton-activated chloride channel contributes to acid-induced cell death in primary rat cortical neurons.Channels (Austin, Tex.) · 2020Article
- Article
- Hypothermia-Induced Ubiquitination of Voltage-Dependent Anion Channel 3 Protects BV2 Microglia Cells From Cytotoxicity Following Oxygen-Glucose Deprivation/Recovery.Frontiers in molecular neuroscience · 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
- TRPM7 is involved in acid-induced necrotic cell death in a manner sensitive to progesterone in human cervical cancer cells.Physiological reports · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The acid-sensitive outwardly rectifying (ASOR) anion channel has been found in non-neuronal cell types and was shown to be involved in acidotoxic death of epithelial cells. We have recently shown that the ASOR channel is sensitive to temperature. Here, we extend those results to show that temperature-sensitive ASOR anion channels are expressed in cortical neurons and involved in acidotoxic neuronal cell death. In cultured mouse cortical neurons, reduction of extracellular pH activated anionic currents exhibiting phenotypic properties of the ASOR anion channel. The neuronal ASOR currents recorded at pH 5.25 were augmented by warm temperature, with a threshold temperature of 26 °C and the Q(10) value of 5.6. After 1 h exposure to acidic solution at 37 °C, a large population of neurons suffered from necrotic cell death which was largely protected not only by ASOR channel blockers but also by reduction of temperature to 25 °C. Thus, it is suggested that high temperature sensitivity of the neuronal ASOR anion channel provides, at least in part, a basis for hypothermic neuroprotection under acidotoxic situations associated with a number of pathological brain states.
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