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
- 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 - The WNK3-SPAK-NKCC1 signaling pathway has been implicated in the pathogenesis of brain injury. The aim of this study is to examine the involvement of this pathway in intracerebral hemorrhage (ICH) and evaluate the therapeutic potential of acupuncture in modulating its activity. A total of 210 Sprague Dawley rats were randomly assigned to experimental groups. ICH was induced in all groups except the sham group via autologous blood injection. Point-through-point acupuncture was administered on the Baihui (GV20) and Qubin (GB7) acupoints. Protein expression levels within the WNK3-SPAK-NKCC1 pathway, as well as inflammatory and apoptotic markers in the perihematomal region, were assessed using western blotting, immunohistochemistry, immunofluorescence co-localization, and enzyme-linked immunosorbent assay. Brain water content, hematoxylin-eosin staining, and neurological function scoring were used to evaluate histopathological changes and functional outcomes. Acupuncture significantly improved neurological function, alleviated cerebral edema, and reduced perihematomal pathological injury in ICH rats at all observed time points. Notably, the therapeutic effect was most pronounced after seven consecutive acupuncture treatments. Time-course analysis of WNK3 and cleaved caspase-3 expression, together with correlation analysis, revealed that the neuroprotective effects of acupuncture were potentially associated with WNK3-mediated apoptotic mechanisms. Based on these findings, day 7 was identified as the optimal time point for further mechanistic investigation. At this time point, continuous acupuncture treatment significantly improved neurological function and decreased brain water content. In addition, the expression levels of WNK3, phosphorylated SPAK and NKCC1, TNF-α, and cleaved caspase-3 were significantly reduced, accompanied by decreased NeuN/TUNEL co-localization (p < 0.05), suggesting that acupuncture may exert neuroprotective effects partly through inhibition of the WNK3-SPAK-NKCC1 signaling pathway. Acupuncture may alleviate brain injury following ICH by suppressing activation of the WNK3-SPAK-NKCC1 signaling pathway, thereby decreasing cerebral edema, inflammatory responses, and neuronal apoptosis. - Source: PubMed
Publication date: 2026/05/25
Zhang Bai-WenZheng LeiKuang Bing-LinZheng JiaYu Xue-PingDai Xiao-HongZou Wei