KCNN4 antibody
- Known as:
- KCNN4 (anti-)
- Catalog number:
- orb101130
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- KCNN4 antibody
Related genes to: KCNN4 antibody
- Gene:
- KCNN4 NIH gene
- Name:
- potassium calcium-activated channel subfamily N member 4
- Previous symbol:
- -
- Synonyms:
- KCa3.1, hSK4, hKCa4, hIKCa1, IK
- Chromosome:
- 19q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-07
- Date modifiied:
- 2019-04-23
Related products to: KCNN4 antibody
Related articles to: KCNN4 antibody
- Breast cancer susceptibility loci identified by genome-wide association studies (GWAS) have revealed extensive genetic contribution to disease risk, yet the genes and immune regulatory mechanisms underlying these associations remain largely unresolved. Here, we integrated immune-cell-specific cis-eQTL data with breast cancer GWAS using a two-sample Mendelian randomization framework. Genetic instruments from five immune-cell resources (DICE, eQTLGen, OneK1K, Soskic, and TenK10K) were evaluated against FinnGen R12 breast cancer summary statistics (24,270 cases and 222,078 controls of European ancestry). Candidate associations were subsequently assessed using Bayesian colocalization, SuSiE fine-mapping, and SMR across independent eQTL datasets and GTEx tissues. TenK10K-based MR identified 516 FDR-significant gene-cell-type associations (131 unique genes), of which 433 associations (106 genes) were supported by convergent genetic evidence (colocalization or LD-based). The APOBEC3A/APOBEC3B locus showed the strongest evidence, where higher immune-cell expression was associated with reduced breast cancer risk. SMR analyses validated 42 of these genes, with YBEY, KCNN4, and ATG10 consistently supported across four independent datasets. In breast tissue, 10 genes showed FDR-significant SMR associations with concordant effect directions. Functional analyses implicated antigen presentation, monocyte differentiation, and APOBEC-mediated DNA editing, with protein-interaction networks converging on the hormone-related genes ESR1 and FGFR2. These findings identify immune-cell-specific regulatory genes that may contribute to breast cancer susceptibility and provide genetically informed candidates for future functional studies. - Source: PubMed
Publication date: 2026/09/24
Han FuleiZhao RongrongYu HainingCui XuehaoNiu Xiao - Cortical spreading depolarization (SD) underlies migraine, frequently co-occurs with seizures, and is associated with poor prognosis after stroke. In rodent models, most genetic therapies for epilepsy suppress seizures by enhancing neuronal K⁺ conductance. Although seizures and SD often co-occur and SD causes temporary neuronal silencing, it remains unknown whether K⁺-conductance-enhancing gene therapy affects SD. Here, we present a genetic method for targeted downregulation of SD using adeno-associated virus to express KCNN4, which encodes the Ca²⁺-gated KCa3.1 channels. We tested the effect of KCNN4 expression in rodent neocortex using patch-clamp electrophysiology, functional imaging in brain slices, and field potential recording in vivo. KCNN4 expression reduced acute seizure-like activity, lowered SD amplitude several-fold both in vivo and in vitro, and slowed SD propagation in brain slices, where epileptiform activity paradoxically reappeared faster after SD. Moreover, SD triggered a Ca²⁺ rebound upon restoration of epileptiform activity, which was counterbalanced by KCa3.1-mediated afterhyperpolarization. Targeted suppression of SD amplitude using KCNN4 expression provides a proof-of-principle for potential gene therapy models for disorders complicated by SD. Reducing SD via increased neuronal K⁺ conductance may have a side effect worth considering in gene therapy for epilepsy, as some literature suggest that SD itself may terminate seizures. - Source: PubMed
Publication date: 2026/09/29
Oblasov Ilya ASmirnova Maria PBorodinova Anastasia AZuzina Alena BSmirnov Ivan ABalaban Pavel MVinogradova Lyudmila VNikitin Evgeny S - Orthodontic tooth movement (OTM) relies on mechanical force that triggers inflammatory responses in periodontal tissue, orchestrating alveolar bone remodeling. Potassium (K) efflux plays a key role in inflammation and tissue remodeling. The calcium-activated potassium channel KCNN4 regulates immune responses, but its role in inflammatory signaling in periodontal ligament cells (PDLCs) under mechanical stress remains unclear. - Source: PubMed
Publication date: 2026/08/21
Zheng FuWang FeifeiChen PengWang PengYang ChenJi ChonghaoWu ZupingFang XinyiYu XinleiXu LehanZhou JingZhang RuiLi GaofengDeng PengChen QianmingChen Xiaoyan - Gardos channelopathy is a rare dehydrated hereditary stomatocytosis caused by gain-of-function KCNN4 mutations. We report a pediatric case due to a recurrent p.Ser314Pro variant, representing the first description outside the Italian population. Over a comprehensive 6-year clinical follow-up, the patient exhibited a stable baseline course punctuated by infection-triggered hemolytic crises, exacerbated by concomitant bronchial asthma. Prospective data demonstrated persistent iron redistribution without systemic overload under conservative management. This case expands the geographic spectrum of the p.Ser314Pro variant, highlights clinical lessons for conservative monitoring, and emphasizes the utility of early next-generation sequencing integration. - Source: PubMed
Publication date: 2026/07/31
Vargas-Pabón ManuelGarcía-Iglesias LorenaCastro-González OlgaHernández-Martín Marco - Cerebral venous sinus thrombosis (CVST) is a critical cause of brain injury and intracranial hypertension. However, its underlying molecular mechanisms remain poorly understood, limiting the development of targeted therapies. This study aims to systematically identify key molecular targets and signaling pathways involved in CVST-induced brain lesions using multi-omics approaches in a modified rat model of CVST. An optimized rat CVST model was established. Cortical tissues were collected from Sham-operated, 2-day post-CVST, and 7-day post-CVST groups for transcriptomic, proteomic, and single-cell transcriptomic sequencing. Bioinformatics analyses were performed to identify differentially expressed genes/proteins, followed by functional enrichment, protein-protein interaction network construction, and hub-gene screening. Further investigations included drug enrichment analysis, molecular docking, and molecular dynamics, as well as the prediction of competing endogenous RNA networks, transcription factor analysis, and expression profiling of potential edema-related therapeutic targets. Multi-omics analyses revealed dynamic changes in gene and protein expression in the brain after CVST, along with associated pathways involved in immune inflammatory responses and tissue repair. Integrative analysis identified 12 core genes (, , , , , , , , , , , and ). Single-cell RNA sequencing validated their expression and delineated cell-type specificity. Molecular docking hinted at the high binding potential of glucocorticoids such as dexamethasone and methylprednisolone to several core targets (, , and ), with all docked complexes showing binding energies below -8.2 kcal/mol. Further molecular dynamics simulations indicated that methylprednisolone forms a stable complex with CD44, driven primarily by van der Waals and electrostatic interactions. Additionally, dynamic levels of several potential edema-related targets (, , , and ) were observed. In summary, by applying integrated multi-omics profiling to a modified rat model, this study systematically mapped the molecular landscape of CVST-induced brain injury. A number of candidate targets and signaling pathways emerged from our analysis, along with several compounds of potential therapeutic interest. Collectively, these results provide a basis for further investigation into the mechanisms underlying CVST and for the design of novel treatment approaches. - Source: PubMed
Publication date: 2026/07/16
Qin XiaohongLu HaoranChen ZhibiaoWang YuxuanChen JiangLiu XizhiZhao ZilongZhou JiaqiTian ShuyueDing Rui