ArticleThe Journal of physiology2013
Stomatin-domain protein interactions with acid-sensing ion channels modulate nociceptor mechanosensitivity.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Identification of molecular nociceptors in Octopus vulgaris through functional characterisation in Caenorhabditis elegans.Biology open · 2026Article
- The mechanotransduction protein STOML3 is required for proprioceptor plasticity following peripheral nerve regeneration.Experimental physiology · 2025Article
- Review
- Proteomic analysis identifies Stomatin as a biological marker for psychological stress.Neurobiology of stress · 2023Article
- Stomatin modulates adipogenesis through the ERK pathway and regulates fatty acid uptake and lipid droplet growth.Nature communications · 2022Article
- Expression pattern of Stomatin-domain proteins in the peripheral olfactory system.Scientific reports · 2022Article
- Force From Filaments: The Role of the Cytoskeleton and Extracellular Matrix in the Gating of Mechanosensitive Channels.Frontiers in cell and developmental biology · 2022Review
- Acid-sensing ion channel 3: An analgesic target.Channels (Austin, Tex.) · 2021Review
- Regulation of acid-sensing ion channels by protein binding partners.Channels (Austin, Tex.) · 2021Article
- Acid-sensing ion channels modulate bladder nociception.American journal of physiology. Renal physiology · 2021Article
- Acid-Sensing Ion Channels and Mechanosensation.International journal of molecular sciences · 2021Review
- DEG/ENaC Ion Channels in the Function of the Nervous System: From Worm to Man.Advances in experimental medicine and biology · 2021Article
- Independent evolution of pain insensitivity in African mole-rats: origins and mechanisms.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2020Review
- Visceral pain from colon and rectum: the mechanotransduction and biomechanics.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Insights into the molecular mechanisms underlying the inhibition of acid-sensing ion channel 3 gating by stomatin.The Journal of general physiology · 2020Article
- Acid-sensing ion channels in sensory signaling.American journal of physiology. Renal physiology · 2020Review
- Stomatin plays a suppressor role in non-small cell lung cancer metastasis.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2019Article
- ASIC3 fine-tunes bladder sensory signaling.American journal of physiology. Renal physiology · 2018Article
- Acid-sensing ion channels: dual function proteins for chemo-sensing and mechano-sensing.Journal of biomedical science · 2018Review
- The Absence of Sensory Axon Bifurcation Affects Nociception and Termination Fields of Afferents in the Spinal Cord.Frontiers in molecular neuroscience · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acid-sensing ion channels (ASICs) and their interaction partners of the stomatin family have all been implicated in sensory transduction. Single gene deletion of asic3, asic2, stomatin, or stoml3 all result in deficits in the mechanosensitivity of distinct cutaneous afferents in the mouse. Here, we generated asic3(-/-):stomatin(-/-), asic3(-/-):stoml3(-/-) and asic2(-/-):stomatin(-/-) double mutant mice to characterize the functional consequences of stomatin-ASIC protein interactions on sensory afferent mechanosensitivity. The absence of ASIC3 led to a clear increase in mechanosensitivity in rapidly adapting mechanoreceptors (RAMs) and a decrease in the mechanosensitivity in both Aδ- and C-fibre nociceptors. The increased mechanosensitivity of RAMs could be accounted for by a loss of adaptation which could be mimicked by local application of APETx2 a toxin that specifically blocks ASIC3. There is a substantial loss of mechanosensitivity in stoml3(-/-) mice in which ∼35% of the myelinated fibres lack a mechanosensitive receptive field and this phenotype was found to be identical in asic3(-/-):stoml3(-/-) mutant mice. However, Aδ-nociceptors showed much reduced mechanosensitivity in asic3(-/-):stoml3(-/-) mutant mice compared to asic3(-/)(-) controls. Interestingly, in asic2(-/-):stomatin(-/-) mutant mice many Aδ-nociceptors completely lost their mechanosensitivity which was not observed in asic2(-/-) or stomatin(-/-) mice. Examination of stomatin(-/-):stoml3(-/-) mutant mice indicated that a stomatin/STOML3 interaction is unlikely to account for the greater Aδ-nociceptor deficits in double mutant mice. A key finding from these studies is that the loss of stomatin or STOML3 in asic3(-/-) or asic2(-/-) mutant mice markedly exacerbates deficits in the mechanosensitivity of nociceptors without affecting mechanoreceptor function.
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