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
- Ischemic stroke (IS) remains a leading cause of global morbidity and mortality, necessitating novel therapeutic targets. MicroRNAs (miRNAs) show promise in modulating post-stroke pathology, yet the role of miR-28-5p in IS remains unexplored. This study aimed to investigate miR-28-5p expression in IS and its clinical and mechanistic significance. - Source: PubMed
Publication date: 2026/03/24
Li ZhuMu JianchangYang HongfeiSun ShuoZhang Yuhao - Hemoglobinopathies are the most common monogenic genetic disorders, primarily managed through blood transfusions or bone marrow transplantation. Clinical severity other than mutational effect not well investigated and still unknown. This study aims to identify dysregulated molecular pathways in red blood cells contributing to thalassemia severity. From a cohort of 285 hemoglobinopathy patients, 10 age-matched individuals with identical compound heterozygous mutations (IVS 1-5 G>C and CD 26 G>A) were screened. Five had severe thalassemia requiring regular transfusions, while five had a non-severe form requiring fewer transfusions. RNA sequencing and proteome analysis were conducted on isolated RBCs, through Novaseq and Orbitrap MS platform respectively. Bioconductor-R and different bioinformatics tools were utilized subsequently. Integrated transcriptome-proteome analysis revealed a global loss of mRNA-protein concordance. CDK11A and MCTS1 lost positive correlation, whereas RLP38 and H3C1 showed compensatory overtranslation, linked to transcription factors regulating erythropoiesis. In TDT, WNK3, HNRNPUL1, COPS7A, and HTATSF1 displayed discordant expression, indicating post-transcriptional aberrations. PTR analysis showed reduced cytoskeletal (ankyrin, spectrin) expression, elevated chaperone activity, ferroptosis markers (FTH1, FTL, HMOX1), and suppressed autophagy. Collectively, these multilayered alterations-splicing dysfunction, post-transcriptional deregulation, ferroptosis, autophagy suppression, oxidative stress, and cytoskeletal fragility-underlie the greater disease severity observed in TDT compared with NTDT. - Source: PubMed
Publication date: 2026/01/30
Mitra NibeditaBhattacharyya UpasanaChowdhury Prosanto KumarPal ArijitKorwar ArvindBhattacharjee SamsidhhiBasu Anupam - Neonatal hypoxic-ischemic encephalopathy (HIE) is brain damage caused by reduced blood/oxygen supply during the perinatal period. There is no adequate treatment currently. The kinase WNK3 is associated with cerebral edema and stroke prognosis, so we assessed its expression in a neonatal rat model of HIE. - Source: PubMed
Publication date: 2025/09/24
Zhang YunfengWang YunWu XiaofengGao HengZhang Ting - Zinc finger homeobox 3 (ZFHX3), a zinc finger homeodomain transcription factor, has been implicated in various brain disorders. However, its molecular mechanism in ischemic stroke remains unknown. In this study, we employed a transient middle cerebral artery occlusion/reperfusion (tMCAO/R) model in C57BL/6 mice and subjected mouse primary pericytes to oxygen-glucose deprivation/reoxygenation (OGD/R) treatment. The results revealed a significant upregulation of ZFHX3 expression in tMCAO/R mice in vivo. ZFHX3 knockdown exacerbated ischemic stroke outcomes, as evidenced by increased cerebral infarction volume, elevated risk of brain hemorrhage, aggravated development of cerebral edema, and worsened blood-brain barrier damage in mice with tMCAO/R. Furthermore, ZFHX3 knockdown inhibited calcium influx thereby attenuating pericyte contraction in mice tMCAO/R model. In vitro studies demonstrated that ZFHX3 knockdown significantly upregulated WNK lysine deficient protein kinase 3 (WNK3) expression in OGD/R-treated pericytes. Conversely, WNK3 knockdown relieved ZFHX3 inhibition-induced pericyte contraction in OGD/R-treated pericytes. In conclusion, our study demonstrates that ZFHX3 silencing may confer neuroprotection in ischemic stroke by suppressing pericyte contraction and calcium influx through inhibition of WNK3 expression. These findings position ZFHX3 as a potential therapeutic candidate for the treatment of ischemic stroke. - Source: PubMed
Publication date: 2025/06/30
Qiu JingWang Yi-HanChen Hui-Sheng - BRAF mutations drive initiation and progression of various tumors. While BRAF inhibitors are effective in BRAF-mutant melanoma patients, intrinsic or acquired resistance to these therapies is common. Here, we identify non-receptor-type protein tyrosine phosphatase 23 (PTPN23) as an alternative effective target in BRAF-mutant cancer cells. Silencing PTPN23 selectively kills BRAF-mutant melanoma cells but not those with wild-type BRAF. Mechanistically, PTPN23, a catalytically inactive phosphatase, intriguingly induces WNK3-mediated phosphorylation of phosphoinositide 3-kinase class II alpha (PI3KC2α) at serine 329, enhancing its catalytic activity. This activation promotes production of PI(3,4)P2 and subsequent AKT2 activation at endosomes to support cell survival. Genetic or pharmacological targeting of the PTPN23-PI3KC2α-AKT2 signaling axis, alone or in combination with BRAF inhibitors, effectively inhibits the growth of BRAF-mutant melanoma and other cancers in vitro and in vivo. We also demonstrate that melanocyte-specific knockout of PTPN23 significantly inhibits BRAFV600E-driven melanomagenesis. Altogether, our findings demonstrate that targeting PTPN23/PI3KC2α offers a new and viable therapeutic strategy for BRAF-mutant cancers. - Source: PubMed
Publication date: 2025/01/22
He YingLi WeiZhang MeilingWang HuiLin PeiluYu YingHuang BinHao MengHe JianuoKong WeiyaoLuo DanXu TengtengWang JiaqiHuang YingZhao QinwenLiu YingZhang JieNian YongZhang LeiZhu BoYin Chengqian