KCNMA1 Rabbit antibody Ab Aff - Purified
- Known as:
- KCNMA1 Rabbit (anti-) Antibody Aff - Purified
- Catalog number:
- AP20653PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- KCNMA1 Rabbit antibody Aff - Purified
Related genes to: KCNMA1 Rabbit 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 Rabbit antibody Ab Aff - Purified
Related articles to: KCNMA1 Rabbit antibody Ab Aff - Purified
- Epilepsy is a prevalent neurological disorder characterized by recurrent seizures and significant impacts on quality of life. This case report describes a 2-year-old male patient presenting with epilepsy associated with fever, in whom whole-exome sequencing (WES) revealed a novel variant in the gene, resulting in the amino acid substitution p.Leu187His. This variant is classified as likely pathogenic and is situated within a key functional domain of the BK channel, a crucial regulator of neuronal excitability. In silico analyses suggest that the substitution alters the local hydrophobicity and may disrupt the channel's function, potentially contributing to the patient's seizure activity. Additionally, the identification of this genetic variant underscores the importance of genetic factors in epilepsy, particularly in cases of drug-resistant epilepsy (DRE) or those with unclear etiology. The findings highlight the utility of WES in diagnosing genetically mediated epilepsy and the need for further research to establish comprehensive genotype-phenotype correlations, ultimately guiding personalized treatment strategies for affected individuals. - Source: PubMed
Publication date: 2026/05/21
Guo WeiSong DakeCheng KeWang ChunhuiWang YujuanYang XiLin YanJiang XunLiu XiyuanLan Li - Tumor cell plasticity and stemness fuel treatment resistance and cancer evolution into often incurable, metastatic terminal disease. To better understand these fundamental aspects of tumorigenesis, here we examine a potential role of KCNMA1, a calcium-activated potassium channel that impacts cell (patho)physiology through membrane functions, in regulating ovarian cancer cell behavior, including plasticity, proliferation, mobility, and response to treatment. Pharmacological activation of KCNMA1 promoted differentiation, while channel blocking induced dedifferentiation and enhanced dissemination potential. Cyclical activation and inhibition potentiated the epithelial/mesenchymal hybrid cell state prone to stemness. KCNMA1 overexpression combined with low-dose channel blockade supported three-dimensional tumor growth. Mechanistically, we found that the balance between cytosolic calcium and potassium, in addition to their absolute levels, governed the observed changes. Our findings support a model in which KCNMA1-mediated regulation of potassium buffers fluctuating calcium signals that drive phenotypic plasticity, thereby stabilizing the epithelial/mesenchymal hybrid state. In addition, KCNMA1 modulation sensitized ovarian cancer cells to standard-of-care chemotherapeutics. Together, this work provides new insights into the role of KCNMA1 and calcium/potassium homeostasis in ovarian cancer cell adaptability, with implications for treatment. - Source: PubMed
Publication date: 2026/06/04
Buchtova TerezaBartkova JirinaYamamoto TatsuroBay Marie LundJensen AllanKjær Susanne KrügerKallunki TuulaBartek JiriStrauss Robert - BK channels, coded by the gene, integrate voltage and intracellular Ca signals and are recognized for their roles in smooth muscle and neuronal excitability. However, their contribution to baseline cardiac physiology remains poorly defined. Here we uncover a fundamental function for BK channels in maintaining normal cardiac performance, independent of pathological stress. Using non-invasive echocardiography, transcriptional profiling, and mechanistic analyses, we demonstrate that deletion disrupts ventricular function, and remodels metabolic and stress-response pathways. Transcriptomic profiling revealed selective downregulation of mitochondrial uncoupling proteins (UCPs) and suppression of the PGC-1α/FOXO3a axis, without broad loss of oxidative phosphorylation components. Enhancing UCP expression restored cardiac performance, indicating that mitochondrial uncoupling and redox control constitute key downstream effectors of BK signaling. Together, these results identify a physiological role for BK channels in maintaining myocardial function and define a mitochondrial BK-UCP axis, critical for cardiac homeostasis. - Source: PubMed
Publication date: 2026/05/22
Rao Shubha GururajaPatel NishiPatel NeelShah KajolHussain AhmedRaut Satish KSingh SwaimanPonnalagu DevasenaAdya SankarAccornero FedericaKohut AndrewSingh Harpreet - 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