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
- 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 - The K2.2 and K3.1 channels are fundamental regulators of membrane potential and calcium signalling and promising targets to treat diseases such as spinocerebellar ataxia and cancer. To fully exploit their therapeutic potential, and to continue studying their pathophysiological role, it is crucial to develop selective modulators for each of these two channels. Here, we present a computational study to identify the molecular determinants behind the selectivity of two recently reported K2.2 modulators, namely, N-(2,1,3-benzoxadiazol-4-yl)-3-(4-methoxybenzene-1-sulfonamido)benzamide and N-(2,1,3-benzoxadiazol-4-yl)-4-(trifluoromethyl)benzamide. We leveraged a protocol combining in silico mutagenesis, molecular dynamics simulations, and protein-ligand docking to analyse the pockets targeted by these ligands. We identified the Ser353/Pro245 substitution to be the main driver of the distinct pocket shapes in K2.2 and K3.1 channels, ultimately defining modulator selectivity. This approach provides novel insights into the structural differences of this binding site across potassium channel subtypes, proposing potential selectivity determinants of the modulators targeting this pocket. - Source: PubMed
Gozzi MatteoMassa JoanaKoch Oliver - This study aims to elucidate the molecular mechanisms through which PET microplastics (PET-MP) influence osteoarthritis (OA) pathogenesis by integrating network toxicology, machine learning, and experimental validation. - Source: PubMed
Publication date: 2026/06/30
Li ZhengtianWang LinHuang HaiquanLu DaoyunHan TingtingZhao JinminDu Gang