KCNMA1 Goat IgG antibody Ab Aff - Purified
- Known as:
- KCNMA1 Goat Immunoglobulin G (anti-) Antibody Aff - Purified
- Catalog number:
- GTX47582
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- KCNMA1 Goat IgG antibody Aff - Purified
Related genes to: KCNMA1 Goat IgG antibody Ab Aff - Purified
- 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 Goat IgG antibody Ab Aff - Purified
Related articles to: KCNMA1 Goat IgG antibody Ab Aff - Purified
- Cellular stiffness impacts multiple steps of cancer metastasis, but mechanisms that regulate the stiffness of cancer cells remain poorly understood. Here, we identified potassium efflux and potassium calcium-activated channel subfamily M regulatory beta subunit 1 (KCNMB1), an auxiliary subunit of the large conductance calcium-activated potassium (BK) channels, as regulators of cellular stiffness downstream of myocardin-related transcription factor A (MRTFA). In primary pericytes, KCNMB1 knockdown increased cellular stiffness, which is consistent with the role of potassium efflux in promoting relaxation during excitation-contraction coupling. In a striking contrast, however, KCNMB1 knockdown decreased cancer cells' stiffness. Softer cancer cells were resistant to natural killer (NK) cell mediated cytotoxicity and the low KCNMB1 expression was associated with reduced survival in breast cancer patients. Importantly, pharmacological activation of BK channels reduced metastatic burden in mice and improved lysis of cancer cells by cytotoxic T lymphocytes. These results highlight the ionic regulation of stiffness in cancer cells and point to BK channel agonism as a therapeutic approach. - Source: PubMed
Publication date: 2026/06/02
Gajda Alexa MHaloul MohamedPai VinayMollaeian KeyvanPatel Khushi JRodríguez-López RaymundoBeverley Katie MSanborn Mark ALee KihakCastillo Caitlyn CWilk Stephanie MWolska Beata MHossen FarukMendenhall Eron NLee James CLevitan IrenaRehman JaleesEr Ekrem Emrah - Osteosarcoma remains aggressive with poor prognosis, particularly in chemotherapy-resistant cases. This study aimed to characterize transcriptional features of chemoresistant osteosarcoma cells, establish a prognostic resistance signature, and identify therapeutic vulnerabilities. Single-cell RNA sequencing (scRNA-seq) was performed on paired pre- and post-neoadjuvant chemotherapy (NAC) specimens from three patients (6 samples; 16,272 cells). Resistance trajectories were reconstructed using Monocle 3 pseudotime analysis. A nine-gene resistance score was validated in the Peking University People's Hospital (PKPH) bulk RNA-seq cohort ( = 70) and Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database ( = 87), with drug sensitivities predicted via oncoPredict. Chemotherapy reduced the malignant cell fraction but triggered expansion of cancer-associated fibroblasts and endothelial cells, creating a stromal-dominant, immune-sparse residual niche. Surviving tumor cells upregulated a nine-gene module along the resistance trajectory: , , , , , , , , and . In an independent unpaired scRNA-seq cohort (two pre- and three post-chemotherapy samples), this signature remained associated with features of chemotherapy resistance. Higher scores correlated with poorer histopathologic response (r = -0.35, = 0.006) and shorter progression-free survival [PKPH: hazard ratio (HR) = 2.4, 95% confidence interval (CI) 1.2-4.8, = 0.01; TARGET: HR = 2.1, 95%CI 1.1-4.0, = 0.02]. Of 198 compounds screened, only Pictilisib, a phosphoinositide 3-kinase (PI3K) inhibitor, showed lower predicted IC50 in the high-score subset across both datasets. However, the paired discovery cohort warrant further validation. Our paired scRNA-seq approach identifies a nine-gene signature linking pre-treatment tumor biology to NAC response and outcome. The enhanced Pictilisib sensitivity in chemoresistant tumors positions PI3K blockade as a strategy meriting prospective testing in refractory osteosarcoma. - Source: PubMed
Publication date: 2026/04/21
Hu LiZhang YaxinWang BoyangLiu QianQi FeiyangLiu HuiminLi QinghuaZhao ZhiqingLiang HaijieLiu XingyuDu ZhiyeWang Jichuan - 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