KCNMA1
- Known as:
- KCNMA1
- Catalog number:
- ARP37677_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- KCNMA1
Related genes to: KCNMA1
- Gene:
- KCNMA1 NIH gene
- Name:
- potassium calcium-activated channel subfamily M alpha 1
- Previous symbol:
- SLO
- Synonyms:
- KCa1.1, mSLO1
- Chromosome:
- 10q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-15
- Date modifiied:
- 2016-10-05
Related products to: KCNMA1
anti-KCNMA1anti-KCNMA1Anti-KCNMA1 AntibodyAnti-Potassium Channel BKCa<_SUB> (High-conductance Ca2+<_SUP>-activated K+<_SUP> Channel, Maxi-K+<_SUP>, Slo, KCNMA1) produced in rabbit AntibodyAnti_Potassium Channel BKCa<_SUB> (High_conductance Ca2+<_SUP>_activated K+<_SUP> Channel, Maxi_K+<_SUP>, Slo, KCNMA1) produced in rabbitBovine Calcium-activated potassium channel subunit alpha-1(KCNMA1) ELISA kitBovine Calcium-activated potassium channel subunit alpha-1(KCNMA1) ELISA kitBovine Calcium-activated potassium channel subunit alpha-1(KCNMA1) ELISA kit SpeciesBovineBovine potassium large conductance calcium-activated channel, subfamily M, alpha member 1 (KCNMA1) ELISA kit, Species Bovine, Sample Type serum, plasmaCanine Calcium-activated potassium channel subunit alpha-1(KCNMA1) ELISA kitCanine Calcium-activated potassium channel subunit alpha-1(KCNMA1) ELISA kitChicken Calcium-activated potassium channel subunit alpha-1(KCNMA1) ELISA kitChicken Calcium-activated potassium channel subunit alpha-1(KCNMA1) ELISA kitChicken Calcium-activated potassium channel subunit alpha-1(KCNMA1) ELISA kit SpeciesChickenChicken potassium large conductance calcium-activated channel, subfamily M, alpha member 1 (KCNMA1) ELISA kit, Species Chicken, Sample Type serum, plasma Related articles to: KCNMA1
- Circulating vasoactive steroids including estrogens, androgens, progesterone, and bile acids modulate the activity of voltage/Ca-gated, big conductance potassium (BK) channels, an action that requires regulatory BK β subunits. In contrast, pregnenolone at local/therapeutic concentrations has recently been shown to modulate BK channel activity in absence of such subunits. The site and mechanism of pregnenolone action remain unknown. Thus, we decided to test the hypothesis that BK channel-forming α subunits (slo1 proteins encoded by KCNMA1 or Slo1 in mammals) contain a specific residue(s) that recognizes pregnenolone and mediates modulation of smooth muscle BK channel activity and diameter of cerebral arteries by this steroid. We used microscale thermophoresis to demonstrate that pregnenolone at local/therapeutic concentrations binds to slo1 proteins at concentrations that inhibit BK channel activity and decrease cerebral artery diameter (K=3.5µM). Based on a slo1 cryo-EM structure (PDB 6V38) computational modeling identified Tyr450, Hys409 and Asp896 as participants in pregnenolone recognition, with hydrogen-arene interactions between steroid and Tyr450. Consistently, slo1Y450F proteins failed to bind pregnenolone. Following heterologous expression, this mutant was resistant to pregnenolone-induced inhibition, an action that was coupled to Ca-driven gating and enabled by the RCK1 high-affinity Ca-binding site. In contrast to their wild-type counterparts, middle cerebral arteries from Kcnma1 Y450F knock-in mice failed to constrict to pregnenolone, whether probed ex vivo or in vivo. Thus, metabolic, circulating, or endothelial factors cannot override pregnenolone cerebrovascular action, which mainly results from direct interaction with Tyr450 within the proximal CRAC motif in the slo1 cytosolic tail domain. Our study provides a new paradigm in vasoactive steroid-BK channel interactions that can be used in developing pharmacophores/new agents to replace/regulate pregnenolone effects in clinical scenarios, and underscores that CRAC motifs may mediate ionotropic receptor regulation by steroids other than cholesterol. - Source: PubMed
Publication date: 2026/08/23
North Kelsey CThapa ShiwaniMysiewicz Steven AShaw AndrewHomanics Gregg EBukiya Anna NDopico Alex M - The Orthobunyavirus genus within the Peribunyaviridae family of enveloped arthropod-borne negative-sense RNA viruses includes species associated with serious or fatal disease in both animals and humans such as Schmallenberg, La Crosse and Oropouche viruses. Orthobunyaviruses (OBVs) are internalized into cells by endocytosis and release their genomes following fusion with late endosome membranes, triggered by low pH of the luminal milieu. There is mounting evidence to suggest OBV endosomal escape is also influenced by potassium ions (K), which increase in concentration as endosomes mature. Endosomal K flux is controlled by cellular K channels, and we previously showed that K channel blockade using broad spectrum pharmacological inhibition abrogates OBV infection, with virions trapped within the endosomes. However, the K channels regulating this process are unknown. Herein, to identify the K channels involved, we studied Bunyamwera virus (BUNV), the prototypical OBV, and screened a siRNA library targeting 342 human ion channels. We identified 19 K channels whose knockdown inhibited BUNV gene expression by over 50%, with at least seven channels affecting BUNV at the entry stage, suggesting they exert a combinatorial influence. Of these seven channels, we used both pharmacological inhibition and genetic channel manipulation to show that OBV escape from CD63-and Rab7-positive late endosomes is controlled by KCNJ2 (K2.1), KCNJ13 (K7.1) and KCNMA1 (BK). These studies add to the understanding of host factors influencing OBV entry, regulation of endosomal ion flux, and could aid in the design or repurposing of therapeutics for the treatment of OBV-associated disease. - Source: PubMed
Publication date: 2026/07/28
Pearson Hayley MHover SamanthaTodd Eleanor J A APanayi KyriakoullaStacey MartinMankouri JamelLippiat Jonathan DHewitt Eric WBarr John N - Severe COVID-19-related acute respiratory distress syndrome (ARDS) often progresses to respiratory failure requiring invasive mechanical ventilation (IMV). Although several biomarkers (e.g., CRP, suPAR, Ang-2) have been explored to predict COVID-19 disease severity, validated early-presentation biomarkers that specifically prognosticate the need for IMV and mechanistic pathways in ARDS remain limited. - Source: PubMed
Publication date: 2026/07/08
Gotur Deepa BGowda Diksha MPinkaew DechaZhang AijunHankins SpencerRodgers ShaefaliXu YitianSyed Mohi UReddy TejaswiniZhao HongZheng JunjunFolz Rodney JMylonakis EleftheriosHamilton Dale J - Imbalance of intestinal mucosal immune regulation is a key mechanism in diarrhea-predominant irritable bowel syndrome (IBS-D). We aimed to characterize this dysregulation in the intestinal mucosa at single-cell resolution. Intestinal mucosal cells from control and neonatal maternal separation-induced IBS-D rats were isolated and subjected to single-cell RNA sequencing (scRNA-seq). Bioinformatics analyses included clustering, differential expression, trajectory inference, and cell-cell communication assessment. We obtained transcriptomes from 4572 high-quality cells, identifying epithelial, stromal, immune, and endothelial lineages. In IBS-D rats, we observed a significant remodeling of the immune compartment, characterized by an increase in monocytes, mast cells, and cycling immune cells, alongside a decrease in T and B lymphocyte subsets. Epithelial cells showed upregulated expression of Krt7 and Foxa3, and downregulated expression of Cst6, Elapor1, and Kcnma1. Cell-cell communication analysis revealed enhanced interactions between epithelial and innate immune cells, involving ligands such as TIGIT. Regulon activity analysis highlighted key transcription factors, including Pax5 in B cells and Mafb in monocytes. Single-cell RNA sequencing reveals that immune barrier dysregulation in the intestinal mucosa of rats with IBS-D is associated with altered immune cell composition, dysregulated expression of epithelial function-related genes, and disrupted intercellular communication, providing novel insights into the pathogenesis of IBS-D. Our high-resolution scRNA-seq atlas delineates the cellular and molecular landscape of intestinal mucosal immune barrier dysfunction in IBS-D, pinpointing novel potential therapeutic targets for this disorder. - Source: PubMed
Publication date: 2026/07/14
Ji LiyanHuang YongquanZhang JiaheLin JiamanYang ZefangYang XilingLiu FengbinHou Qiuke - Olfactory dysfunction is a debilitating condition with no established treatment. This study evaluated the efficacy of intranasal (i.n.) NAD administration in restoring olfactory function. Cultured human olfactory stem cells (hOSCs) were treated with NAD and assessed by immunofluorescence staining, PCR, and western blot analyses. In vivo, mice with ZnSO-induced anosmia were treated with i.n. NAD, intraperitoneal dexamethasone, or PBS and evaluated by histological analysis, behavioral tests, bulk RNA-sequencing (RNA-seq), and in situ hybridization. NAD promoted hOSC differentiation into olfactory sensory neurons (OSNs), evidenced by increased stem cell (SOX2 and nestin) and OSN markers (Tuj1 and OMP) expression, and upregulated neuronal differentiation-related genes (SOX2, NESTIN, NEUROD1, NEUROG1, and OMP). In vivo, the NAD group showed significant olfactory function improvement and marked olfactory epithelium repair. Bulk RNA-seq of the olfactory turbinate tissue identified 113 differentially expressed genes (cluster T1) upregulated in control and NAD groups. The Gene Ontology (GO) term "modulation of chemical synaptic transmission" was associated with cluster T1, and 25 genes implicated in this GO were upregulated in the NAD group. Integration with publicly available single-cell RNA-seq data identified six neuronal marker genes - ABHD2, DLGAP2, FOXO3, HIPK2, KCNMA1, and PCDH17 - upregulated by NAD. Protein expression of DLGAP2 and PCDH17 was higher in differentiated hOSCs treated with NAD. In situ hybridization confirmed that Dlgap2, Foxo3, and Pcdh17 expression was restored in anosmic mice treated with i.n. NAD. The potential therapeutic efficacy of i.n. NAD administration was demonstrated by showing regeneration of OSNs in hOSCs and restoring olfactory function in an anosmia mouse model. - Source: PubMed
Publication date: 2026/07/01
Yoo Shin HyukJang Jung YeonBae Jun-SangVentura ReizaKim Eun HeeKim A YoungMo Ji-HunPark JaewooKang KyuhoYun YeogyunLee Jun HeeKim Yong-JaeLee Dong-JoonKim Ji Heui