ASIC3 [DRASIC], antiserum, guinea pig, 150 ul.
- Known as:
- ASIC3 [DRASIC], antibodies, guinea pig, 150 ul.
- Catalog number:
- GP14105-150
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- ASIC3 [DRASIC] antiserum guinea pig 150 .
Related genes to: ASIC3 [DRASIC], antiserum, guinea pig, 150 ul.
- 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: ASIC3 [DRASIC], antiserum, guinea pig, 150 ul.
(+)- USNIC ACID AR CAS: 7562-61-0(Arg8)-Vasopressin - Diluted Antiserum for RIA(Arg8)-Vasopressin - Diluted Antiserum for RIA,(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Immunofluorescence Kit, Host Guinea Pig(Arg8)-Vasopressin - Immunofluorescence Kit, Host: Guinea Pig(Arg8)-Vasopressin - Immunofluorescence Kit, Host: Guinea Pig(Arg8)-Vasopressin - Purified Antiserum - IgG(Arg8)-Vasopressin - Purified Antiserum - IgG, Host Rabbit(Arg8)-Vasopressin - Purified Antiserum - IgG, Host Rabbit Related articles to: ASIC3 [DRASIC], antiserum, guinea pig, 150 ul.
- Platelets are key mediators of hemostasis and thrombosis. Acid-sensing ion channel 3 (ASIC3), a proton-gated cation channel, can be activated at neutral pH by the synthetic compound 2-guanidine-4-methylquinazoline (GMQ). However, the role of GMQ in platelet activation and its potential dependence on ASIC3 remain unclear. This study investigated whether GMQ modulates platelet function at physiological pH (7.4), whether this regulation is mediated by ASIC3, and what the underlying molecular mechanisms are. We found that GMQ significantly suppressed platelet activation in both human and murine platelets at pH 7.4 and attenuated thrombus formation and hemostatic function in mice. ASIC3 was confirmed to be functionally expressed in human and murine platelets. Although ASIC3 deficiency did not affect basal platelet characteristics or platelet activation at pH 7.4, it markedly diminished GMQ-mediated suppression of platelet activation, thrombosis, and hemostasis. Mechanistically, GMQ enhanced cyclic adenosine monophosphate (cAMP) production and promoted protein kinase A (PKA) Thr197 phosphorylation through interaction with ASIC3-cyclase-associated protein 1 (CAP1), thereby suppressing platelet function. Overall, this study demonstrates, for the first time, that GMQ inhibits platelet activation and thrombosis under physiological pH by targeting ASIC3 and activating the CAP1/cAMP/PKA signaling pathway. These findings suggest that targeting the non-proton domain of ASIC3 at physiological pH may represent a novel and promising antiplatelet therapeutic strategy. - Source: PubMed
Publication date: 2026/05/30
Zhang PengLiu PengYu HanwenLiu DongshengWei MengZhang KandiHuang JianpengLi YingSu YuanyuanZhang TiantianZhang Junfeng - Acid-sensing ion channel 3 (ASIC3) is a promising therapeutic target for pain because of its unique peripheral expression profile in somatosensory neurons and channel properties for sensing mild extracellular acidosis associated with inflammation, ischemia, and metabolic changes. - Source: PubMed
Publication date: 2026/05/29
Chi Chih-HungLee Cheng-HanChen Chih-Cheng - Acid-sensing ion channels (ASICs) are excitatory ligand-gated ion channels directly gated by extracellular protons. Proton-sensitivity of ASICs is subject to modulation by different compounds, for example neuropeptides and lipids. In this study, we uncovered that the currents of the two most proton-sensitive ASICs, homomeric ASIC1a and ASIC3, are strongly potentiated by thyroid hormones, particularly triiodothyronine (T3). Potentiation by T3 had micromolar affinities and rapid on- and offset kinetics. Moreover, T3 did not affect gramicidin A-induced currents, suggesting that thyroid hormones had direct action on ASICs, indicating that they are a new class of allosteric ASIC modulators. Interestingly, for ASIC1a, T3 increased the efficacy of protons, whereas for ASIC3, it increased potency of protons. These results suggest that thyroid hormones could modulate ASIC activity in particular brain regions where their concentration is sufficiently high. - Source: PubMed
Publication date: 2026/05/27
Qin LuWiemuth DominikGründer Stefan - IntroductionEpithelial-mesenchymal transition (EMT) is a key driver of tumor invasion and metastasis, which is closely associated with poor prognosis in patients with surgically resected lung cancer. Hypercapnic acidosis (HCA) is a common comorbidity in various lung diseases; however, its specific role in regulating EMT in lung cancer remains unclear. Acid-sensing ion channel (ASIC) genes have been implicated in tumor progression, but their expression patterns and prognostic value in lung cancer, as well as their involvement in HCA-mediated EMT regulation, require further investigation.MethodsThe expression levels of ASIC genes and their prognostic significance were analyzed in lung adenocarcinoma and lung squamous cell carcinoma using the Gene Expression Profiling Interactive Analysis (GEPIA) database. A549 lung cancer cells were exposed to HCA conditions (10% CO, pH 6.69 ± 0.02) for five days to induce EMT phenotypes. Cell proliferation, migration, and invasion capacities were evaluated using corresponding functional assays. The expression levels of EMT-related markers (E-cadherin and vimentin) and ASIC3 were quantified by immunohistochemical staining, western blot analysis, and reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR). Additionally, amiloride was used to inhibit ASIC3 expression to verify its regulatory role in HCA-induced EMT.ResultsBioinformatics analysis showed that overexpression of ASIC3 mRNA was significantly correlated with reduced overall survival in lung cancer patients ( < .05). In vitro experiments demonstrated that HCA exposure significantly upregulated ASIC3 expression ( < .01) and promoted EMT in A549 cells, as evidenced by downregulated E-cadherin expression and upregulated vimentin expression. Moreover, HCA significantly enhanced the migration and invasion abilities of A549 cells ( < .01). Importantly, inhibition of ASIC3 expression by amiloride reversed all these HCA-induced effects, including the alterations in EMT markers and the enhancement of cell migratory/invasive capacities.ConclusionThe HCA microenvironment induces EMT in A549 lung cancer cells through the activation of ASIC3. These findings suggest that ASIC3 may serve as a potential therapeutic target for the treatment of lung cancer, which could help improve clinical outcomes by inhibiting tumor invasion and metastasis mediated by EMT. - Source: PubMed
Publication date: 2026/03/19
Zhao LifangZhang LihongLuo ChunyanFang XingjunYuan PeihuaQu LiangchaoFu Huan - Cardiac afferent neurons have been shown to trigger overactivation of neurohormonal systems known to drive adverse cardiac remodeling following myocardial infarction (MI). Acid-sensing ion channels (ASICs) that are highly expressed in cardiac sympathetic afferents sense ischemia-induced myocardial acidosis. We hypothesized that genetic deletion of ASICs might abrogate disadvantageous remodeling after MI by disrupting afferent signaling pathways otherwise resulting in overactivation of neurohormonal responses. To test this, we induced MI in wild type (WT) and ASIC3 mice and assessed cardiac remodeling by serial echocardiography. We found that ASIC3 mice had less LV dilation relative to ischemic zone fraction, increased LV mass and wall thickness, and increased stroke volume compared to WT mice after MI. To investigate a potential role of the autonomic nervous system, we measured renal and splanchnic sympathetic nerve activity (SNA), heart rate and systolic blood pressure variability (sBPV), and hemodynamic responses to atropine and propranolol. Following MI, ASIC3 mice had lower baroreceptor-renal SNA reflex sensitivity than WT mice, associated with elevated sBPV. Our data show that ASIC3 plays an important role in cardiac remodeling after MI potentially via modulation of baroreflex sensitivity and sBPV. ASIC3 may be further investigated as a potential therapeutic target in heart failure. - Source: PubMed
Monaghan Karley MGibbons David DWard Chad CEl-Geneidy MaramKutschke William JZimmerman Kathy AMorgan Donald AStauss Harald MHarding Anne Marie SBader Michelle C MSnyder Peter MSabharwal RasnaWeiss Robert MRahmouni KamalBenson Christopher J