Ask about this productRelated genes to: WNK3 antibody
- Gene:
- WNK3 NIH gene
- Name:
- WNK lysine deficient protein kinase 3
- Previous symbol:
- PRKWNK3
- Synonyms:
- -
- Chromosome:
- Xp11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-07
- Date modifiied:
- 2014-11-19
Related products to: WNK3 antibody
Related articles to: WNK3 antibody
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by prominent neuroinflammation. Microglia, the resident immune cells of the central nervous system, play a key role in AD-associated neuroinflammation, yet the molecular mechanisms regulating their inflammatory activation remain incompletely understood. In this study, we integrated human single-nucleus RNA sequencing with computational analyses and experimental validation to identify potential regulators of inflammatory microglial states in AD. Microglial subpopulations were characterized, and pseudotime analysis was performed to infer transcriptional state transitions across neuropathological stages. High-dimensional weighted gene co-expression network analysis (hdWGCNA) and machine learning were used to prioritize candidate genes for functional validation. KLHL2 was identified as a candidate regulator, and its expression progressively decreased along the inferred pseudotime trajectory, with concordant decreases in Klhl2 mRNA and KLHL2 protein levels observed in APP/PS1 mice and Aβ42-stimulated BV2 cells. In contrast, WNK3 expression level increased without corresponding changes in Wnk3 mRNA. In BV2 cells, Klhl2 overexpression reduced WNK3 expression level, JNK and c-Jun phosphorylation, and pro-inflammatory mediator expression, whereas Klhl2 knockdown produced the opposite effects. Collectively, these findings support KLHL2 as a negative regulator of microglial inflammatory activation and suggest the involvement of WNK3/JNK/c-Jun signaling in this process. - Source: PubMed
Publication date: 2026/09/09
Yang YaoDai ConghuiXu ZongtangZhuo LinpeiXiang KunLin XiaoouSun JingLiu JiamingTong Qiuling - With the widespread application of microwave technology in communication and medical fields, concerns regarding its biosafety, particularly the effects on the central nervous system, have increased. The brain is considered a sensitive target organ for microwave radiation; however, the molecular mechanisms underlying microwave-induced cognitive impairment remain unclear. The purpose of this study was to evaluate the effects of 4.3 GHz microwave radiation at different power densities on spatial learning and memory in mice, and to identify key molecular changes in the hippocampus associated with cognitive impairment. Mice (male, C57BL/6N) were exposed to 4.3 GHz microwave radiation at power densities of 10 or 30 mW/cm for 30 min. Spatial learning and memory abilities were assessed using the Morris water maze (MWM). The hippocampal structure was assessed by HE staining at multiple time points following microwave exposure. Integrated RNA-sequencing (RNA-seq) and 4D-data-independent acquisition (4D-DIA) analyses of the hippocampus were performed at 6 h after microwave exposure, and differentially expressed molecules were selected and validated by quantitative polymerase chain reaction (qPCR) and parallel reaction monitoring (PRM). The 4.3 GHz microwave exposure significantly prolonged escape latency in the MWM, indicating impaired spatial learning or navigation ability. Histological examination revealed transient neuronal damage in the hippocampal CA1 and CA3 regions. Multi-omics analysis and subsequent validation revealed molecular alterations. Following microwave radiation, the expression of synaptic plasticity-related genes and was significantly upregulated. At the protein level, significant downregulation was observed for Protein sidekick-2 and IQGAP1, while WNK3 was significantly upregulated. In summary, 4.3 GHz microwave exposure impaired spatial learning or navigation ability, accompanied by structural damage in the hippocampus and molecular alterations in synaptic plasticity-related pathways. , , Protein sidekick-2, WNK3, and IQGAP1 might serve as candidate molecules for understanding and mitigating microwave-induced cognitive deficits. - Source: PubMed
Publication date: 2026/07/06
Qian TingtingCheng WenjingSong LequanDong JiWang HaoyuZhang JingZhao LiWang HuiPeng Ruiyun - Porcine Sertoli cells (SCs) treated by acute heat stress (HS) (43°C, 0.5 h) have significantly decreased taurine level. Taurine treatment of porcine SCs could promote proliferation, inhibit apoptosis, enhance mitochondrial function and modulate protein profile. However, whether taurine can alleviate damages of porcine SCs caused by acute HS is unknown. We here showed that treatment of porcine SCs using taurine (5.7 μM) for 12 h before acute HS (HS0.5-B12-Taurine) significantly rescued damages induced by acute HS (HS0.5-Control), including cell viability, proliferation, apoptosis, intracellular reactive oxygen species (ROS) levels, mitochondrial number, and lactate content. Transcriptome sequencing identified 18 differentially expressed genes (DEGs) (HS0.5-B12-Taurine vs. HS0.5-Control), mainly enriched in Gene Ontology (GO) terms of apoptosis, transmembrane transport, inward rectifier potassium channel activity, and 2 iron/2 sulfur cluster binding. RT-qPCR validated expression of 5 DEGs (GRIA4, KCNJ13, PTER, RAB44 and SLC12A8) and 7 other genes (AFF4, CXCL8, DENND5B, EPM2AIP1, SLC6A6, SSH2 and WNK3), most of them showing change trend consistent with RNA-seq results. Moreover, HDAC5 was confirmed to be significantly reduced in HS0.5-B12-Taurine (Western blotting: P < 0.05; Immunofluorescence: P < 0.01). Collectively, these findings suggest that taurine protects porcine SCs against damages induced by acute HS. - Source: PubMed
Publication date: 2026/07/23
Liu Xiao-YingHao Ruo-BingWang Xin-XinYin ZongjunDu Zhi-QiangYang Cai-Xia - Gliomas are highly prevalent and lethal primary malignant tumours of the central nervous system. MicroRNA plays a tumour-suppressive role in various tumours, including glioma. This study aims to elucidate the expression profile, clinical relevance, biological roles, and underlying mechanisms of miR-1305 in glioma. - Source: PubMed
Publication date: 2026/06/24
Wang YongGuo Mengnan - WNK kinases are chloride- and osmotic-stress-regulated protein kinases recently shown to be controlled by potassium. Prior studies demonstrated the direct binding of chloride and osmotic stress-related water in WNK kinase regulation. Here, we probe potassium binding and regulation of WNK kinases via crystallography coupled with mutagenic analysis of WNK kinase autophosphorylation and activity. Crystals of unphosphorylated WNK1 grown in cesium formate, a surrogate for potassium, yielded nonsulfur scattering peaks at 5.75 keV. Mutations were introduced into amino acids flanking the anomalous diffraction peaks. Mutations in WNK1/E388 and the corresponding WNK3/E314, probing a peak close to WNK1/I384, led to reduced inhibition by potassium while maintaining kinase autophosphorylation and substrate phosphorylation activity. Other peaks probed by mutagenesis either did not bear out as potassium regulatory sites or were not validated due to the inactivity of the mutants synthesized. Previously synthesized chloride- and water-binding mutants demonstrate correlated sensitivity to chloride and potassium. Potassium, chloride, and water are all WNK inhibitors that share a common mechanism binding the same low-activity asymmetric dimer of WNK1 kinase domains. - Source: PubMed
Publication date: 2026/05/26
Goldsmith Elizabeth JPleinis John MWagner ArminMykhaylyk VitaliyAkella RadhaHumphreys John MHe HaixiaNorrell LoganMorrison Daryl ERodan Aylin R