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
- Osteoarthritis (OA) is a chronic whole-joint disease involving extracellular matrix remodeling, inflammatory signaling, immune-stromal interactions, and sensory-associated processes. MicroRNAs (miRNAs) may contribute to post-transcriptional regulation within these interconnected molecular domains, but concurrent mRNA and miRNA expression patterns remain insufficiently characterized in naturally occurring canine OA. A total of 12 formalin-fixed, paraffin-embedded (FFPE) canine tissue specimens were classified as osteoarthritic joint tissues (OA; n = 7) and control joint tissues without radiographic or histopathological evidence of OA (C-JT; n = 5). RT-qPCR was used to quantify 17 selected mRNAs involved in extracellular matrix remodeling, chronic inflammatory signaling, immune-stromal interactions, and neuroinflammatory and sensory-associated processes, together with five miR-30 family members. Statistical comparisons were performed on ΔCq values using two-sided unpaired Welch's -tests followed by Benjamini-Hochberg false discovery rate correction. Compared with C-JT, OA tissues showed significantly higher expression of ADAMTS5, MMP2, MMP13, COL2A1, SPARC, HP, VEGFA, IGFBP6, and ASIC3 after false discovery rate correction. MMP9, IL1B, IL1R1, IL1RAP, JAK2, TYK2, NGFB, and NTRK1 did not differ significantly between the two joint-tissue groups. MiR-30b was significantly downregulated in OA, whereas miR-30c, miR-30d, and miR-30e were significantly upregulated; miR-30a did not differ significantly. Exploratory database-supported miRNA-gene connectivity was used for candidate prioritization but was not interpreted as evidence of direct regulation in canine joint tissue. Canine osteoarthritic capsulosynovial tissues exhibit concurrent alterations in selected mRNAs and miR-30 family members across matrix-remodeling, immune-stromal, and sensory-associated molecular domains. These findings identify OA-associated expression patterns but do not establish pathway activation, direct miRNA-mRNA regulation, or disease progression. They provide a focused molecular basis for future mechanistic studies of post-transcriptional regulation in naturally occurring canine OA. - Source: PubMed
Publication date: 2026/09/09
Guelfi GabriellaRatto Vicente FCapaccia CamillaCiancabilla FrancescoForti DavidLeonardi LeonardoBufalari AntonelloLiso ArcangeloMaranesi Margherita - 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