Ask about this productRelated genes to: KCNN4 antibody
- Gene:
- KCNN4 NIH gene
- Name:
- potassium calcium-activated channel subfamily N member 4
- Previous symbol:
- -
- Synonyms:
- KCa3.1, hSK4, hKCa4, hIKCa1, IK
- Chromosome:
- 19q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-07
- Date modifiied:
- 2019-04-23
Related products to: KCNN4 antibody
Related articles to: KCNN4 antibody
- Over the past five decades, air pollution has posed a growing threat to human health, particularly affecting the respiratory system. This study aims to investigate the potential molecular mechanisms underlying the relationship between exposure to air pollutants and the development of COPD and to identify potential gene targets that may play a key role in this process. In this study, researchers used several publicly available databases to obtain target genes related to air pollutants and COPD, determine the overlapping genes between them and performed GO and KEGG enrichment analyses to elucidate the underlying mechanisms. Cross-validation was performed using multiple datasets from the Gene Expression Omnibus (GEO) database to screen out candidate targets, and molecular docking techniques were utilized to investigated molecular interactions between candidate targets and air pollutants. Candidate targets were subsequently validated and analyzed using immune cell infiltration analysis, single-cell transcriptome data, risk prediction model construction and clinical data to further elucidate their relationship with COPD. Findings suggest that HDAC9, DPP9 and KCNN4 are candidate targets of air pollutants that are potentially involved in COPD development. These results offer new insights into the potential molecular mechanisms linking air pollution exposure to COPD and underscore the need for further in-depth research on air pollution issues. - Source: PubMed
Song DongXie LinGao XuegeChen YushanZhong ChunjunLi HuicongZhan ShaofengLian Leshen - Hypertension-induced erectile dysfunction is associated with endothelial dysfunction in the corpus cavernosum. Membrane depolarization activates the NLRP3 inflammasome, with downregulation of endothelial Ca-activated K channels type 2.3 (K 2.3) and upregulation of endothelin-1 (ET-1) linked to erectile dysfunction. However, underlying mechanisms remain incompletely understood. We hypothesized that activating K 2.2/2.3 channels reverses erectile dysfunction and ET-1-induced NLRP3 activation in hypertensive DOCA/salt mice. Hypertension was induced in mice using a DOCA/salt model, with unilaterally nephrectomized mice as controls. We measured blood pressure, intracavernous pressure (ICP), and corpus cavernosum (CC) contractility, and performed immunoblots for K 2.3, caspase-1, and interleukin-1β (IL-1β). DOCA/salt mice showed impaired erectile function and increased IL-1β activity and reduced K 2.3 expression. Treatment with the endothelin receptor antagonist bosentan or the K 2.2/2.3 channel opener NS13001 reversed these dysfunctions and reduced ET-1-induced NLRP3 activation. NS13001 also restored decreased currents in endothelial cells exposed to ET-1. These findings establish that hypertension-induced erectile dysfunction involves an ET-1/membrane depolarization/NLRP3 inflammasome axis in corpus cavernosum endothelial cells, and that targeting endothelial K 2.2/2.3 channels represents a promising therapeutic strategy to counteract erectile dysfunction. - Source: PubMed
Publication date: 2026/03/13
Sobrano Fais RafaelComerma-Steffensen Simon GabrielPinilla EstefanoMatchkov Vladimir VTostes RitaSilva Carneiro FernandoSimonsen Ulf - Myocardial fibrosis is a pivotal pathological component of the failing heart where the sympatho-β-adrenergic receptor (β-AR) signaling is augmented. Intermediate-conductance Ca-activated K channel (K3.1) is expressed in fibroblasts and mediates fibrosis, but the regulation of K3.1 expression by β-AR activation remains unclear. Used for treatment of skin diseases, dimethyl fumarate (DMF) is recently found to suppress transcription cofactor yes-associated protein (YAP). Here, we examined whether DMF ameliorates myocardial fibrosis induced by β-AR activation through inhibiting YAP-mediated K3.1 expression in fibroblasts. - Source: PubMed
Publication date: 2026/03/18
Wu Lin-HongBai Ru-YueChen Jia-YiPang Zheng-DaHai Xia-XiaHan Meng-ZhuanYang Yi-YiWang YanZhang YiZhang JieShe GangDu Xiao-JunDeng Xiu-Ling - Dehydrated hereditary stomatocytosis (DHSt) is a heterogeneous group of rare hemolytic disorders with autosomal dominant inheritance. A series of 20 cases demonstrates that early identification of DHSt can prevent unnecessary interventions and improve the management of anemia, iron overload, and other complications in pediatric and adult patients. The presence of elevated mean corpuscular hemoglobin concentration (MCHC) with resistant erythrocytes suggested a possible association with variants in PIEZO1. Patients with KCNN4 variants showed no clear signs of erythrocyte dehydration, but, as with PIEZO1, macrocytosis, hemolytic anemia, and iron overload were common manifestations. - Source: PubMed
Publication date: 2026/03/19
Rossetti EstefaníaEandi Eberle SilviaAguirre FernandoNieto LeandroFernández DiegoMininni María FMilanesio BereniceMasegosa EugeniaPepe CarolinaÁvalos Vanesa - KCa3.1 encodes the intermediate-conductance calcium-activated potassium channel KCa3.1, a regulator of membrane potential and calcium-dependent signalling in cardiovascular and immune cells. Increasing evidence indicates that KCa3.1 is a shared driver of vascular remodelling, inflammation, fibrosis, and electrical instability across multiple cardiovascular diseases. In ischaemic heart disease (IHD), KCa3.1 is upregulated in endothelial cells, vascular smooth muscle cells, macrophages, and T lymphocytes, where it promotes smooth muscle proliferation, neointimal formation, and chronic vascular inflammation. Genetic deletion or pharmacological blockade of KCa3.1 reduces atherosclerotic plaque burden and restenosis in animal models. In atrial fibrillation (AF), KCa3.1 contributes to electrical remodelling by shortening atrial action potential duration and to structural remodelling by driving fibroblast activation and collagen deposition. KCa3.1 also regulates macrophage polarisation and pro-inflammatory cytokine release in atrial tissue, linking immune activation to arrhythmogenic substrate formation. Inhibition of KCa3.1 prolongs atrial refractoriness, attenuates atrial fibrosis, and reduces AF inducibility in multiple preclinical models. Emerging data in valvular heart disease suggest that KCa3.1 is upregulated in valvular interstitial cells and regions of active calcification, where it supports myofibroblast differentiation, osteogenic signalling, and inflammatory crosstalk, implicating the channel in fibrocalcific valve degeneration. Collectively, these findings position KCa3.1 as a central molecular integrator of electrical, fibrotic, and inflammatory pathways in cardiovascular disease. The availability of selective KCa3.1 inhibitors with established human safety profiles supports the feasibility of therapeutic translation. Targeting KCa3.1 may enable disease-modifying strategies that extend beyond symptom control to suppress maladaptive cardiovascular remodelling. - Source: PubMed
Publication date: 2026/02/27
Antoun IbrahimLayton Georgia RSomani RiyazNg G AndréBradding PeterZakkar Mustafa