Kcnma1
- Known as:
- Kcnma1
- Catalog number:
- 065281A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- 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
- Large-conductance Ca²⁺- and voltage-activated K⁺ (BK) channels are critical regulators of neuronal excitability and have been implicated in multiple epileptic syndromes. Their functional diversity arises from the co-assembly of pore-forming α-subunits with auxiliary β subunits, among which β4 is highly expressed in distinct regions of the central nervous system, including hippocampal Dentate Gyrus Granule Cells (DGGCs). Here, we identify montelukast (MTK), a clinically approved cysteinyl-leukotriene receptor antagonist, as a direct activator of BK channels, with markedly enhanced efficacy in the presence of the β1 and β4 subunits. MTK acts at submicromolar concentrations and facilitates channel opening by altering the energetics of the pore domain, independent of voltage-sensor activation or Ca²⁺ binding to the cytosolic gating ring. In mouse hippocampal slices, MTK reduces intrinsic excitability of DGGCs by decreasing input resistance and enhancing the afterhyperpolarization, effects fully reversed by the BK channel blocker paxilline. Experiments using physiological DGGCs action potential voltage waveforms confirm that MTK enhances subthreshold and evoked BK currents in α/β4 channels as selective targets. Altogether, our findings suggest that MTK, beyond its known anti-inflammatory properties, may modulate neural excitability through direct BK channel activation, offering a novel therapeutic strategy for seizure suppression. - Source: PubMed
Publication date: 2026/05/05
Orsi FedericoMonat JulianaEnrique NicolásMilesi VerónicaCastillo KarenRaingo JesicaMartín Pedro - To summarize the clinical features and genetic variation spectrum of children with paroxysmal kinesigenic dyskinesia (PKD) admitted to the Children's Medical Center of Union Hospital Affiliated to Fujian Medical University and to provide references for clinical diagnosis and genetic counseling. - Source: PubMed
Publication date: 2026/04/09
Zheng Li-PingYe Yun-PengWang Su-PingLin Xiao-XiaHu Jun - Pancreatic cancer is one of the most lethal malignancies worldwide, characterized by late diagnosis, aggressive progression, and poor survival. Dysregulation of regulated cell death (RCD) pathways, including apoptosis, ferroptosis, necroptosis, and mitochondrial dysfunction, contributes to tumor survival, therapy resistance, and immune evasion. Understanding the molecular mechanisms underlying these processes is critical for identifying prognostic biomarkers and therapeutic targets. Publicly available pancreatic cancer gene expression datasets (GSE227567 and GSE275246) were analyzed to identify differentially expressed RCD and mitochondrial genes. FRGs, APGs, NRGs, and MGs were intersected with the DEGs, followed by functional enrichment, protein-protein interaction (PPI) network construction, and hub gene prioritization. Co-expression, immune infiltration, and pathway activity analyses were performed across pathological stages and pan-cancer datasets. Missense SNPs in top hub genes ATF4 and PMAIP1 were evaluated for structural and energetic impact using HOPE and DynaMut. Analysis identified 448 FRGs, 73 APGs, 32 NRGs, and 930 MGs in GSE227567, and 123 APGs, 0 FRGs, 36 NRGs, and 577 MGs in GSE275246. Cross-dataset overlap was highest for APGs (116 genes), while other RCD and mitochondrial genes were largely dataset-specific. Filtering and PPI network analysis prioritized nine hub genes (ATF4, PMAIP1, BCL2L1, ATF3, TRADD, SRC, SFN, KCNMA1, GUK1). Functional enrichment highlighted mitochondrial metabolism, oxidative phosphorylation, and apoptosis pathways, with integration into PI3K-AKT, MAPK, p53, and VEGF signaling. Immune infiltration analysis revealed myeloid-enriched tumor microenvironments in mutant contexts. Pan-cancer and stage-wise expression profiling indicated that ATF4 and PMAIP1 exhibit consistent stage-dependent modulation. Survival analysis showed that high PMAIP1 expression correlates with poor prognosis (HR = 1.26, p = 0.00185), while ATF4 shows a protective trend (HR = 0.84, p = 0.0145). SNP analysis revealed six missense variants in each gene, with ATF4 variants predominantly destabilizing and affecting the bZIP domain, whereas PMAIP1 variants were mostly surface-exposed and modulatory. Our integrative analysis identifies ATF4 and PMAIP1 as key RCD- and mitochondrial-associated genes in pancreatic cancer, with functional SNPs that influence prognosis and may serve as therapeutic targets. These findings provide insights into mitochondrial-driven apoptosis, tumor progression, and potential avenues for precision medicine interventions. - Source: PubMed
Publication date: 2026/04/23
Ali Syed LuqmanAli AwaisKhatrawi Elham MohammedKiran RafiaKhan Bilal - Indigenous poultry genetic resources are crucial for breeding and food security. In Xinjiang, China, the Ili gamecock and Yemili chicken represent two indigenous breeds with distinct and valuable traits. The Ili gamecock is prized for its large body size and aggressive behavior, whereas the Yemili chicken shows remarkable adaptation to the cold environment of the Tacheng area, with strong disease resistance, and foraging ability suited to free-range grazing. As understanding their genetic basis is key to their conservation and sustainable use, we conducted whole-genome sequencing of 22 individuals from both breeds and integrated the data with 83 publicly available genomes to construct a comprehensive dataset of 12 global chicken populations. After identifying over 11.3 million high-quality SNPs, we assessed genetic diversity and population structure. Analyses revealed that the Ili gamecock is closely related to the Turpan gamecock, forming a distinct cluster. Selection signature analyses based on fixation index (FST) and nucleotide diversity ratio (π ratio) identified genomic regions under positive selection associated with aggressiveness and muscularity in gamecocks (e.g., NELL1, SOX5, SEMA3A, KCNMA1) and with stress response, intestinal integrity, and energy homeostasis in Yemili chickens (e.g.,MAPK8IP3, HBEGF, PARD3, ATP6V1B2, ATP5PD). This study provides a comprehensive genomic landscape of these two emerging Xinjiang breeds, elucidates their unique evolutionary histories, and offers valuable genetic resources for future conservation and breeding programs. - Source: PubMed
Publication date: 2026/03/21
Yang HaichenLiang QianqianSu PengAndersson GöranBongcam-Rudloff ErikRouzi MahabaJiang LinHan JilongYang Min - Inherited ion channel gene mutations cause network synchronization disorders, but their early impact on circuit development is less understood. Childhood absence epilepsy features cortical spike-wave discharges driven by thalamocortical rebound bursting. Loss-of-function mutations in P/Q-type calcium channels impair neurotransmitter release yet paradoxically increase thalamic excitability. In tottering mice, global P/Q deficiency elevates T-type calcium and big potassium (BK) channel transcripts in thalamic relay neurons, increasing excitability before seizure onset and coincident with the N-to-P/Q exocytosis switch. Selective P/Q deletion in cortical L6 pyramidal presynaptic input to thalamus reproduced the coordinate transcript elevation, indicating a transsynaptic mechanism. Unexpectedly, tottering, but not L6 mutants, showed increased thalamic neurogenesis and β-catenin/Lef1 upregulation, linking intrinsic thalamic P/Q channel function to early structural brain development. These findings reveal that subtle inherited changes in P/Q-mediated transmitter release and postsynaptic membrane calcium dynamics disrupt a previously unrecognized embryonic homeostatic pathway regulating growth, plasticity, and excitability in thalamocortical circuits. - Source: PubMed
Publication date: 2026/04/02
Thompson Samantha JMiao Qing-LongSonig AnikaNoebels Jeffrey