ACCN1 antibody
- Known as:
- ACCN1 (anti-)
- Catalog number:
- orb1004
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- ACCN1 antibody
Related genes to: ACCN1 antibody
- Gene:
- ASIC2 NIH gene
- Name:
- acid sensing ion channel subunit 2
- Previous symbol:
- ACCN, ACCN1
- Synonyms:
- ASIC2a, BNC1, BNaC1, hBNaC1, MDEG
- Chromosome:
- 17q11.2-q12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-22
- Date modifiied:
- 2018-02-13
Related products to: ACCN1 antibody
Related articles to: ACCN1 antibody
- Acid-sensing ion channels (ASICs) are proton-gated members of the degenerin/epithelial sodium channel family that are emerging as multifaceted regulators of cardiovascular function. ASICs expressed in baroreceptor, cardiac, and skeletal muscle afferents contribute to reflex control of blood pressure, cardiac function, and sympathetic outflow. In vascular smooth muscle and endothelial cells, ASICs integrate mechanical, metabolic, and humoral signals to regulate vascular tone. In the systemic circulation, ASIC2 contributes to pressure-dependent vasoconstriction of renal and cerebral arteries, supporting blood flow autoregulation and protection against organ injury. In contrast, ASIC1a promotes vasodilation, contributing to nitric oxide-dependent dilation in the cerebral arteries and to endothelium-dependent hyperpolarization and vasodilation in mesenteric arteries. In the pulmonary vascular smooth muscle cells, ASIC1a plays a central role in acute hypoxic- and receptor-mediated vasoconstriction, a role that becomes increasingly important in chronic hypoxia-induced pulmonary hypertension. Under these conditions, metabolic reprogramming drives extracellular acidification and enhances ASIC1a trafficking to the plasma membrane, promoting sustained depolarization, augmented store-operated calcium entry, and a hyperproliferative, apoptosis-resistant smooth muscle phenotype. ASIC1a additionally regulates mitochondrial homeostasis by modulating mitochondrial membrane potential, redox balance, and apoptotic susceptibility. Chronic hypoxia redistributes ASIC1a from mitochondria to the plasma membrane, leading to mitochondrial dysfunction and cell survival signaling, key features of pulmonary vascular disease. This review summarizes current understanding of ASIC function in the systemic and pulmonary vasculature and highlights non-proton-mediated signaling mechanisms, emerging mitochondria-specific mechanisms, sex-related differences, and therapeutic opportunities and challenges in targeting ASIC-dependent signaling pathways in vascular disease. - Source: PubMed
Publication date: 2026/07/13
Jernigan Nikki L - ASIC2 and ENaC subunits are required for stretch-induced mechanoreceptor currents in renal vascular smooth muscle cells and pressure-induced constriction responses in small renal arteries and arterioles. To examine whether ENaC subunits and ASIC2 can form mechanosensitive ion channels, we co-expressed ASIC2a with ENaC β and γ subunits in Xenopus oocytes to test the channel's response to flow-induced shear stress by changing the perfusion rates with Na as the conducting ion. Under baseline conditions (0.5 ml/min), oocytes co-expressing ASIC2a and β/γENaC (ASIC2a+β/γENaC) displayed larger inward Na currents than ASIC2a alone. In oocytes expressing ASIC2a+β/γENaC, but not ASIC2a alone, baseline currents increased in response to a fast perfusion (5 ml/min). The inward Na currents carried by ASIC2a+β/γENaC were insensitive to 10 μM amiloride but were inhibited when extracellular Na was replaced with NMDG. A gain-of-function ASIC2a mutant, ASIC2aG430V, had readily detectable amiloride-sensitive baseline currents. Interestingly, flow-mediated channel activation was dependent on subunit composition. A high perfusion rate (5 ml/min) elicited a two-fold increase in Na currents in oocytes expressing ASIC2aG430V or ASIC2aG430V+βENaC, which was further increased to approximately four-fold when γENaC or both β and γ subunits were co-expressed with ASIC2aG430V (ASIC2aG430V+γENaC or ASIC2aG430V+β/γENaC). Exposure to acidic pH evoked greater channel activity in oocytes expressing ASIC2aG430V+β/γENaC than ASIC2aG430V alone. In contrast, ENaC β and γ subunits did not alter the channel's permeability to monovalent cations of different sizes. Collectively, our experimental findings and structural modeling suggest that ASIC2a assembles with ENaC β and γ subunits to form mechanosensitive channels. - Source: PubMed
Publication date: 2026/05/14
Shi ShujieWhelan Sarah Christine MSzekely Kennedy GKashlan Ossama BDrummond HeatherKleyman Thomas R - Ocean acidification presents a significant threat to marine life, yet its neurobiological mechanisms remain poorly understood. This study examined how acid-sensing ion channels (ASICs) mediate neuronal excitability and anxiety-like behaviour in marine medaka (Oryzias melastigma) under elevated CO concentrations (1000 and 1900 ppm). Transcriptomics revealed early upregulation of asic1a (4 days), while RT-qPCR demonstrated increased asic1a, asic1b, asic2 and asic4a (7 days), with only asic1a sustained at 30 days. Immunofluorescence confirmed heightened Asic2 in emotion-processing brain regions following acidification. Transmission electron microscopy unveiled distinct ultrastructural alterations: widened synaptic clefts, thinned postsynaptic densities, and decreased mitochondrial aspect ratios. Mitochondrial membrane potential assays revealed a reduction in membrane potential in response to acidification. Electrophysiological recordings showed increased neuronal firing count in the dorsolateral telencephalon under acidification, behavioural assessments revealed significant anxiety-like phenotypes, effects that were fully rescued by ASIC inhibition. These results indicated that temporal specificity in ASIC subtype expression in acidification response. The interplay of synaptic and mitochondrial dysfunction, neuronal hyperexcitability, and behavioural alterations suggested acidification impaired both synaptic transmission efficiency and mitochondrial function, destabilizing neural circuits. This study systematically elucidates the neurotoxic effects of ocean acidification on marine fish, providing critical scientific evidence for predicting the ecological impacts of climate change on marine organisms. - Source: PubMed
Publication date: 2026/04/10
Liu WenxiaoGong ZhaofeiNiu HaoCui JinghuiWang Xiaojie - Glioma, the most frequent primary intracranial tumor, is characterized by infiltrative growth in the central nervous system, pronounced invasiveness, high malignancy, and poor clinical prognosis. The existing treatment methods include surgery, radiotherapy and chemotherapy, but the efficacy is still limited. Analysis of The Cancer Genome Atlas (TCGA) dataset reveals marked downregulation of acid-sensing ion channel 2 (ASIC2) expression in glioma tissues, which significantly correlates with reduced patient survival. Moreover, ASIC2 expression is inversely associated with the extent of immune cell infiltration and glioma stem cell markers. Functional experiments demonstrate that both knockdown and overexpression of ASIC2 critically regulate glioma cell proliferation, invasion, and metastatic potential through mechanisms mediated by matrix metalloproteinase 2 (MMP2), calcineurin, and nuclear factor of activated T cells 1 (NFAT1) signaling pathways. These findings delineate a pivotal role for ASIC2 in governing glioma malignant behavior and establish its relevance as a potential molecular target for therapeutic intervention. - Source: PubMed
Publication date: 2026/01/28
Tian WenxiuWang YuWang ZhenmingPeng FujunSun JiayiQi HuiminZhang ZhaoruiWang PingQiao SenWang HongmeiDong Junhong - Acid-Sensing Ion Channel 2 (ASIC2) has been implicated in mechanosensation. We reported previously that ASIC2 is highly expressed in aortic baroreceptor neurons and contributes to baroreceptor mechanotransduction; and that ASIC2 deficient mice exhibit decreased baroreflex sensitivity (BRS), sympathovagal imbalance and neurogenic hypertension. Oxidative stress is widely considered an important contributor to hypertension. The major goal of this study was to determine if treatment of ASIC2 mice with the antioxidant tempol attenuates baroreflex/autonomic dysfunction and hypertension. Blood pressure (BP), heart rate (HR) and locomotor activity were measured by telemetry in conscious, control C57BL/6 and ASIC2 male mice, before and after administration of tempol in drinking water (1 mM) for two weeks. Cardiac sympathetic tone, mean arterial BP and BP variability were higher, and cardiac vagal tone and BRS were lower in ASIC2 mice, compared with controls (P < 0.05). Oxidative stress measured by mRNA expression of NADPH oxidase subunits (Nox2, Nox4, p22phox) and dihydroethidium (DHE) fluorescence was increased significantly (P < 0.05) in ASIC2 mice in a tissue-specific manner (sympathetic and nodose ganglia > > brain stem > > skeletal muscle, with no change in aorta). Treatment with tempol strongly attenuated DHE fluorescence and restored autonomic regulation and BP to control levels in ASIC2 mice, while not affecting these phenotypes in control mice. We conclude: (1) oxidative stress in ASIC2 mice is prominent in the autonomic nervous system but not present in aorta; and (2) the antioxidant tempol reverses decreased BRS, sympathovagal imbalance and hypertension in ASIC2 mice; effects that are associated with decreased oxidative stress. - Source: PubMed
Publication date: 2025/12/19
Sabharwal RasnaAbboud Francois MChapleau Mark W