Acid-sensing ion channels (ASICs) are trimeric proton-gated sodium channels. Recently it has been shown that these channels play a role in necroptosis following prolonged acidic exposure like occurs in stroke. The C-terminus of the channel is thought to mediate necroptotic cell death through interaction with receptor interacting serine threonine kinase 1 (RIPK1). This interaction is hypothesized to be inhibited at rest via an interaction between the C-terminus and the N-terminus which blocks the RIPK1 binding site. Here, we use a combination of two transition metal ion FRET methods to investigate the conformational dynamics of the termini while the channel is closed and desensitized. We do not find evidence that the termini are close enough to be bound while the channel is at rest and find that the termini may modestly move closer together when desensitized. At rest, the N-terminus adopts a conformation parallel to the membrane about 10 Å away. The distal end of the C-terminus may also spend time close to the membrane at rest. After acidification, the proximal portion of the N-terminus moves marginally closer to the membrane whereas the distal portion of the C-terminus swings away from the membrane. Together these data suggest that a new hypothesis for RIPK1 binding during stroke is needed.
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http://dx.doi.org/10.1101/2023.07.05.547693 | DOI Listing |
FASEB J
January 2025
School of Pharmacy, Anhui Medical University, Hefei, China.
The activation of acid-sensing ion channel 1a (ASIC1a) in response to extracellular acidification leads to an increase in extracellular calcium influx, thereby exacerbating the degeneration of articular chondrocytes in rheumatoid arthritis (RA). It has been suggested that the inhibition of extracellular calcium influx could potentially impede chondrocyte ferroptosis. The cystine transporter, solute carrier family 7 member 11 (SLC7A11), is recognized as a key regulator of ferroptosis.
View Article and Find Full Text PDFToxicology
January 2025
Department of Physiology & Institute of Neuroscience, School of Basic Medical Science, Hengyang Medical College, University of South China, Hengyang, 421001, Hunan, People's Republic of China. Electronic address:
Although it has been confirmed that acid-sensing ion channel 1 (ASIC1) plays a critical role in acidosis-induced neuronal injury and death, its underlying mechanisms remain largely unclear. In the present study, we investigated the involvement of ASIC1 in acidosis-induced neuronal death and its underlying mechanisms in HT22 neurons. The neurons were cultured in acidic medium to mimic extracellular acidosis.
View Article and Find Full Text PDFNeuropharmacology
December 2024
Department of Pharmacology, Medical School of Southeast University, Nanjing, China. Electronic address:
Epilepsy, a prevalent neurological disorder characterized by spontaneous recurrent seizures, significantly impacts physiological and cognitive functions. Emerging evidence suggests a crucial role for metabolic factors, particularly lactate, in epilepsy. We discuss the applicability of the astrocyte-neuron lactate shuttle (ANLS) model during acute seizure events and examine lactate's metabolic adaptation in epilepsy progression.
View Article and Find Full Text PDFAcid-sensing ion channels (ASICs) are typically activated by acidic environments and contribute to nociception and synaptic plasticity. ASIC1a is the most abundant subunit in the central nervous system and forms homomeric channels permeable to Na and Ca , making it a compelling therapeutic target for acidotic pathologies including stroke and traumatic brain injury. However, a complete conformational library of human ASIC1a in its various functional states has yet to be described.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Department of Anesthesiology, The Affiliated Baiyun Hospital of Guizhou Medical University, Guiyang, Guizhou Province, China.
Background: Acid-sensing ion channels are activated during myocardial ischemia and are implicated in the mechanism of myocardial ischemia-reperfusion injury (MIRI). Acid-sensing ion channel 3 (ASIC3), the most pH-sensitive member of the ASIC family, is highly expressed in myocardial tissues. However, the role of ASIC3 in MIRI and its precise effects on the myocardial metabolome remain unclear.
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