ACCN3
- Known as:
- ACCN3
- Catalog number:
- 000996A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACCN3
Related genes to: ACCN3
- Gene:
- ASIC3 NIH gene
- Name:
- acid sensing ion channel subunit 3
- Previous symbol:
- ACCN3
- Synonyms:
- TNaC1, DRASIC
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-04
- Date modifiied:
- 2016-10-05
Related products to: ACCN3
Related articles to: ACCN3
- The acid-sensing ion channel 3 (ASIC3) is a neuronal voltage-insensitive Na channel located in the peripheral nervous system (PNS) and activated by extracellular H, that is dysregulated in peripheral neuropathic pain. ASIC3 was found in stem cells of central nervous system (CNS)-located glioblastoma multiforme (GBM CSCs), and its chronic activation kills dysfunctional GBM CSCs without any effect on ASIC3-lacking CNS tissues. We rationally designed and synthesized blood-brain barrier (BBB)-compliant analogues of GMQ, a known guanidyl quinazoline ASIC3 activator; we replaced its guanidine group with a guanyl hydrazone (GH) and carried out scaffold substitutions and other structural variations in 16 GMQ analogues to establish a structure-activity relationship (SAR). Our more potent GH analogue 1a showed specific activity against GBM CSC neurospheres, coupled with a better safety profile on mammalian nontumor cells and a better brain-to-plasma ratio compared with GMQ. Such results provide valuable insights for further structural optimization of heteroaryl GHs as ASIC3 modulators. - Source: PubMed
Maiorana LeonardoCollura NicolettaGotti AndreaDe Leonardis GiuliaDonati GretaMaiocchi AliceMarinelli LucianaMenegon AndreaSeneci Pierfausto - DC. (), the sole official species in the 2025 Chinese Pharmacopoeia, is a subtropical woody vine endemic to southern China. Its traditional ethnomedicinal uses for pain, inflammation, and metabolic disorders are supported by modern extraction technologies-ultrasonic-assisted extraction (UAE), microwave-assisted extraction (MAE), flash extraction, and enzymatic hydrolysis-that enhance the recovery of bioactive constituents. Phytochemical profiling reveals over 60 pentacyclic triterpenoid saponins, phenylpropanoids, flavonoid glycosides, and acidic polysaccharides. Pharmacological mechanisms include COX-2 inhibition, TRPV1 blockade, and ASIC3 downregulation for analgesia and anti-inflammation; AMPK/IRS-1 pathway activation for antitumor and metabolic effects; enhancement of superoxide dismutase (SOD) activity for antioxidant activity; and Bax/Bcl-2 modulation for hepatoprotection. Food applications include enzyme-assisted juice, fermented vinegar, clarified wine, and spray-dried powders. This review synthesises botany, phytochemistry, pharmacology, and processing innovations, highlighting its commercial potential and proposing metabolomic strategies for discovering novel bioactive compounds to accelerate its integration into nutraceutical and medicinal formulations. - Source: PubMed
Publication date: 2026/08/23
Chang Chen-YuWang Xiao-YunLiu Ke-JiaLi QiLu Shu-YanMa Qin-GeWei Rong-Rui - Acid-sensing ion channel 3 (ASIC3), a proton-gated cation channel predominantly expressed in primary afferent nociceptors, is an acidosis-related pain generator. Previous experiments suggested that ASIC3 is also involved in the generation of itch. However, mechanistic links between ASIC3 and itch, including the expression of ASIC3 in itch-mediating primary sensory neurons, remain unclear. We examined ASIC3 expression in these sensory neurons and then investigated whether mild acid stimulation could induce ASIC3-dependent itch without overt pain in mice. - Source: PubMed
Publication date: 2026/07/30
Shibata YasuhiroChaya RyosukeYokoi YutoKumamoto NatsukoUeda TakashiYousif Elamin Yousif ZobidahFujihara YoshitakaIkawa MasahitoYasui TakahiroUgawa Shinya - Cytokine interleukin-33 (IL-33) signaling in primary sensory neurons plays a crucial role in pain. However, the underlying molecular mechanisms remain poorly understood. Therefore, we investigated whether IL-33 signaling affects ion channels in nociceptive dorsal root ganglion (DRG) neurons. Herein, we reported that the application of IL-33 enhanced the electrophysiological activity of acid-sensing ion channels (ASICs). IL-33 dose-dependently increased acid-evoked ASIC currents in mouse DRG neurons. IL-33 enhanced the maximum responses of ASICs, whereas the sensitivity to acidic stimuli remained unaffected. This IL-33-induced enhancement of ASIC currents was dependent on suppression of the tumorigenicity 2 (ST2) receptors. The enhancing effect of IL-33 on ASIC currents was prevented by the p38 mitogen-activated protein kinase inhibitor SB202190, but not by the ERK inhibitor U0126 or the JNK inhibitor SP600125, indicating the effect was p38-dependent. Moreover, IL-33 potentiated the action potential triggered by acidic stimuli. Finally, ASIC3-deficient mice displayed attenuated mechanical hyperalgesia induced by intraplantar or intramuscular injection of IL-33. Our findings revealed that IL-33 enhanced ASIC function via ST2 and the intracellular p38 signaling pathway, which might provide a promising therapeutic approach for pain treatment by targeting IL-33/ST2 signaling. - Source: PubMed
Publication date: 2026/08/07
Liu Ting-TingLi Xue-MeiQiu Chun-YuHu Wang-Ping - Leukotriene B4 (LTB4) is a lipid mediator generated from arachidonic acid. Studies have shown that LTB4 plays a role in the pain process. However, little is known about the underlying molecular and cellular mechanisms. The present data demonstrated a functional link between LTB4 and acid-sensing ion channels (ASICs) in mouse dorsal root ganglion (DRG) neurons. LTB4 potentiated acid-activated ASIC currents in a concentration-dependent and pH-independent manner. The potentiating effect of LTB4 on ASIC currents was mediated by BLT1 receptors but not by BLT2 receptors. The LTB4-induced potentiation of ASIC currents was prevented by the ERK1/2 inhibitor U0126 and the JNK inhibitor SP600125, but not by the p38 inhibitor SB202190, indicating involvement of intracellular ERK1/2 and JNK signaling. Moreover, LTB4 potentiated the burst of action potentials evoked by acidic stimuli in mouse DRG neurons. Behaviorally, intraplantar injection of LTB4 exaggerated spontaneous nociceptive behaviours evoked by subsequent acid challenge in WT mice, and developed attenuated mechanical hyperalgesia in ASIC3 KO mice. Our results suggested that LTB4 potentiated the electrophysiological activity of ASICs via BLT1 receptors as well as the ERK1/2 and JNK signaling pathways, which might open promising new perspectives for pain treatment associated with tissue acidification. - Source: PubMed
Publication date: 2026/07/29
Sun FeiYuan HuanWang ChenDu BeibeiLi Xue-MeiLiu Ting-TingQiu Chun-YuHu Wang-Ping