KCNMA1
- Known as:
- KCNMA1
- Catalog number:
- NB300-554
- Product Quantity:
- 0.1 mg
- 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
- 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 - Adequate renal perfusion is critical for maintaining kidney function, and its impairment contributes significantly to acute kidney injury (AKI) and related cardiovascular complications. Dopamine (DA) is clinically employed to improve renal perfusion, but its efficacy remains controversial due to paradoxical vasoconstriction at higher doses. - Source: PubMed
Publication date: 2026/06/22
Kang XuyaJin HanZheng YaoyaoZhang KejiaZhu GuangxuanWang XinyingXu ChaojieZhang ChiHe LeiYu ZhuoyangXue GenlongLiu LijunZhang YanYao LinDong ErdanLiu Yahan - Atrial fibrillation (AF) is the most common cardiac arrhythmia. Although familial AF frequently follows an autosomal dominant inheritance pattern, the genetic mechanisms remain incompletely defined. We sought to identify the causal variant within a previously established linkage region on chromosome 10q22-q24. - Source: PubMed
Publication date: 2026/06/09
Martínez-Moreno RebeccaPérez-Serra AlexandraShah GopiRoura ElisabetRigat Pujolàs AlbertIglesias AnnaDel Olmo BernatHong KuiRioux John DScornik Fabiana SPérez Guillermo JRoberts RobertBrugada Ramon - 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