Ask about this productRelated genes to: KCNN3 Blocking Peptide
- Gene:
- KCNN3 NIH gene
- Name:
- potassium calcium-activated channel subfamily N member 3
- Previous symbol:
- -
- Synonyms:
- KCa2.3, hSK3, SKCA3
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-07
- Date modifiied:
- 2016-02-04
Related products to: KCNN3 Blocking Peptide
Related articles to: KCNN3 Blocking Peptide
- Anorexia nervosa (AN) is a severe metabo-psychiatric disorder with the highest mortality rate among psychiatric conditions. Its characteristic onset during adolescence suggests that disrupted neurodevelopmental processes during critical periods may contribute to disease pathophysiology. In this exploratory study, we conducted an integrated multi-layered omics analysis to identify molecular alterations affecting neurodevelopmental pathways in individuals with AN. We employed three complementary approaches: DNA methylation sequencing via Reduced Representation Bisulfite Sequencing (RRBS), microRNA (miRNA) expression profiling using panel-based qPCR, and microbiome characterization through 16S rRNA sequencing in a sample of 38 patients with AN and 40 healthy controls. Analyses focused on molecular mechanisms involved in neurodevelopmental processes. RRBS analysis identified methylation differences in neurodevelopmentally relevant genes, particularly (voltage-gated calcium channel) and (transcription factor). miRNA profiling revealed extensive dysregulation, with 74 miRNAs showing altered levels in the AN pools. Network analysis highlighted that miR-135 family targets (SK3 channel involved in neuronal excitability), while miR-374b regulates (IGF-1 signaling modulator). Microbiome analysis revealed that 42% of the AN group exhibited dramatic oral dysbiosis characterized by Proteobacteria dominance. Our findings demonstrate coordinated multi-level dysregulation of mechanisms governing neural circuit maturation during adolescence, supporting a neurodevelopmental framework for understanding AN. The convergence of molecular alterations on ion channels and growth factor signaling suggests systems-level perturbations in developmental regulatory mechanisms. The identified miRNAs represent potential biomarkers and therapeutic targets, while microbiome heterogeneity suggests distinct clinical subgroups. While exploratory in nature, this work provides novel insights into AN molecular architecture and generates testable hypotheses for future mechanistic studies incorporating individual-level data essential to validate these candidates and establish robust clinical correlations. - Source: PubMed
Publication date: 2026/05/19
Gilardini FedericaSabatucci AnnalauraCifani CarloSegura-Garcia CristinaPucci MariangelaRania MariannaD'Addario Claudio - Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiovascular conditions, which may be linked to ion channel dysfunction. In decades, Genetic studies in HCM patients have shown that multiple gene mutations in potassium and calcium ion channels, which may contribute to HCM progression. The direct relationship between HCM and ion channels still needs to be clarified. - Source: PubMed
Publication date: 2026/05/04
Li ShaohuaXu JingqiZhang FengXu QingLao DonghuiZhang TianyuYe YanrongTian Yuan - Dysfunction of endothelial cells manifests early in pulmonary arterial hypertension and represents a critical therapeutic target. Nevertheless, the limited efficacy of single-target interventions underscores the need for innovative strategies that enable precise therapeutic modulation. - Source: PubMed
Publication date: 2026/05/13
Yang ShayingWang ZhiweiYang TengLiu YuanYu FanMao AiqinFeng LeiWen XinTang ChunleiMa Xin - Ponatinib, a third-generation BCR::ABL1 inhibitor, has antileukemic activity but is associated with cardiovascular toxicity, for which transcriptome-level responses remain incompletely characterized. Here, we defined a ponatinib-associated transcriptomic signature and examined its mechanistic implications using two public RNA sequencing (RNA-Seq) datasets: GSE186341 (11 cancer cell lines treated with kinase inhibitors) and GSE217421 (induced pluripotent stem cell (iPSC)-derived cardiomyocytes treated with approved drugs). Principal component analysis (PCA) and -means clustering were used to define expression-based subgroups of vehicle-treated (DMSO) controls. DESeq2, followed by fixed-effect meta-analysis, estimated subgroup-specific treatment effects and pooled effect estimates across subgroups. In GSE186341, we identified 2639 meta-analytic differentially expressed genes (meta-DEGs). Among these, 81 genes were also differentially expressed in GSE217421 after ponatinib treatment, identifying an overlapping gene set across datasets. In contrast, imatinib showed no overlap with these 81 genes under the same cross-dataset analysis framework. Cardiotoxicity-relevant functions were represented by directionally consistent genes linked to cardiac repolarization-associated ion handling (), insulin-responsive metabolic regulation (, ), cyclic adenosine monophosphate (cAMP)-responsive stress signaling (), and mitochondrial homeostasis and redox regulation (, ). Collectively, these results define a ponatinib-associated transcriptomic signature and nominate cross-dataset transcript-level candidates for subsequent mechanistic and experimental validation in ponatinib-associated cardiotoxicity. - Source: PubMed
Publication date: 2026/04/30
Kong JoonhoJang JaeyeonKong Jee HyunLee Taesic - The metastasis of hepatocellular carcinoma (HCC) cells remains a major obstacle to achieving favorable clinical outcomes, yet the underlying molecular mechanisms are still not fully understood. The dysregulation of ion channels is related to epithelial-mesenchymal transition (EMT) phenotype-related pathways, especially the aberrant function of K+ ion channels in HCC. In this study, we observed that the potassium-calcium-activated channel subfamily N member 3 (KCNN3/SK3/ KCa2.3) ion channels were significantly upregulated in HCC cells, promoting the migration and invasion of HCC in vitro and in vivo. Mechanistically, activation of the KCNN3 ion channel was found to enhance phosphorylation of the CCCTC-binding factor (CTCF), which in turn stimulates transcription of the EMT-related factor special AT-rich sequence-binding protein 1 (SATB1) via binding the "CCCTC" region within its promoter, thereby driving HCC cell migration and invasion. Furthermore, we identified that speckle-type POZ protein (SPOP), an E3 ligase adaptor, recognizes the SPOP-binding consensus (SBC) motif "ASSTT" (aa 250-254) in KCNN3 and mediates its ubiquitination via K27-linked ubiquitin chain. Notably, this type of ubiquitination does not induce KCNN3 turnover, but induced KCNN3 translocation from the cell membrane into the cytosol, thus suppressing KCNN3-mediated ion channel activity. Importantly, HCC-associated SPOP mutations or KCNN3-ΔSBC dramatically disrupt the SPOP-KCNN3 regulatory axis, accelerating HCC progression. These effects can be effectively counteracted by treatment with the KCNN3 channel inhibitor edelfosine and the calcium chelators BAPTA-AM, suggesting a promising therapeutic strategy for HCC patients. - Source: PubMed
Publication date: 2026/05/10
Zhan ZiqingGe YidongShi JiaxinLiang HongzeLi YuxuanJin JiabeiChen GunZhai FengguangKong LiliLin YanWang SiyuanChen LitaoLiu LinlinChen KuihaoLou PengrongYe MengJin Xiaofeng