KCNMA1 Antibody (OALA01589)
- Known as:
- KCNMA1 Antibody (OALA01589)
- Catalog number:
- oala01589
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KCNMA1 Antibody (OALA01589)
Ask about this productRelated genes to: KCNMA1 Antibody (OALA01589)
- 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 Antibody (OALA01589)
Related articles to: KCNMA1 Antibody (OALA01589)
- 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 - 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
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