WNK2 control peptide
- Known as:
- WNK2 reference short protein sequence
- Catalog number:
- WNK21-P
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- WNK2 control peptide
Related genes to: WNK2 control peptide
- Gene:
- WNK2 NIH gene
- Name:
- WNK lysine deficient protein kinase 2
- Previous symbol:
- SDCCAG43, PRKWNK2
- Synonyms:
- NY-CO-43, KIAA1760
- Chromosome:
- 9q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-07
- Date modifiied:
- 2016-10-05
Related products to: WNK2 control peptide
Related articles to: WNK2 control peptide
- Schizophrenia is a chronic, debilitating psychiatric disorder with high heritability. We have previously established Arhgap10 S490P/NHEJ (Arhgap10) mice, a schizophrenia-related mouse model carrying Japanese schizophrenia patient-derived ARHGAP10 variants. These mice exhibited activated Rho-kinase (ROCK) signaling, schizophrenia-related behavioral and neurobiological phenotypes that were ameliorated by the ROCK inhibitor fasudil. Although phospho-signaling is increasingly implicated in schizophrenia pathophysiology, comprehensive phosphoproteomic profiling in the brain of Arhgap10 mice has not yet been performed, leaving key downstream ROCK-dependent targets unidentified. Here, we conducted unbiased phosphoproteomic analysis of the medial prefrontal cortex (mPFC) of wild-type (WT) and Arhgap10 mice, treated with or without fasudil. We identified 15 phosphoproteins that were significantly upregulated in the mPFC of Arhgap10 mice compared with WT controls. Among these, phosphorylated microtubule-associated protein tau at serine 404 (pTau_S404), phosphorylated autophagy-related protein 9 A at serine 828 (pATG9A_S828), and phosphorylated serine/threonine-protein kinase WNK2 at threonine 282 (pWNK2_T282) were markedly reduced to control levels by fasudil treatment. Upstream kinase enrichment analysis, together with targeted validation, revealed alterations in the AKT/GSK3β signaling node as the context for these fasudil-responsive candidates. Since these phosphoproteins are linked to autophagy-related processes, we further examined autophagy-lysosome-associated readouts. Arhgap10 mice showed autophagy-associated alterations in the mPFC, while fasudil increased autophagosome- and autolysosome-associated vesicle puncta in primary cortical neurons. This study provides the first phosphoproteomic network map of the mPFC in the Arhgap10 mouse model of schizophrenia, identifying ROCK-responsive phosphoproteins along with autophagy-associated alterations and fasudil-responsive changes. - Source: PubMed
Publication date: 2026/04/25
Zhu WenjunTanaka RinakoMatsuzaki TetsuoNakai TsuyoshiNagai TakuNabeshima ToshitakaKaibuchi KozoOzaki NorioIkesue HiroakiMizoguchi HiroyukiYamada Kiyofumi - Ovarian cancer (OC) remains the most lethal gynecologic malignancy. Our previous work showed that WNK lysine-deficient protein kinase 2 (WNK2) promotes OC cell proliferation and migration. To clarify the molecular basis of WNK2-driven OC progression, here, we performed transcriptome sequencing to identify WNK2-regulated mRNAs and noncoding RNAs. We validated candidate targets using qRT-PCR and Western blot analyses. Functional assays, including CCK-8, colony formation, and Transwell assays, evaluated the role of POU5F1B and its capacity to rescue the effects of WNK2 knockdown. POU5F1B is a promising OC therapeutic target, mediating WNK2-driven oncogenesis in xenograft models (n = 10). Because AKT acts downstream of POU5F1B, we examined AKT phosphorylation and found that POU5F1B displayed clear oncogenic activity in OC cells. WNK2 upregulated POU5F1B mRNA and protein levels, while POU5F1B overexpression reversed the tumor-suppressive effects caused by WNK2 depletion. Mechanistically, WNK2 silencing decreased AKT phosphorylation, which POU5F1B overexpression restored. Together, these results demonstrate that WNK2 promotes OC progression by upregulating the validated oncogene POU5F1B and activating AKT signaling. These findings establish WNK2 as an oncogenic driver and a promising therapeutic target in OC. - Source: PubMed
Publication date: 2026/02/02
Li FengjieJia YongqinMin XiaoliZhang PangyangLi YudiLi DengCao LanqinWang YanzhouLiang Zhiqing - Endometriosis is a chronic estrogen-dependent disorder affecting up to 10% of women of reproductive age, and the absence of reliable noninvasive diagnostic tools contributes to delayed diagnosis and disease progression. To identify potential biomarkers, we profiled miRNA expression in serum, saliva, and vaginal mucus from 20 women (10 with endometriosis and 10 controls) using next-generation sequencing. Differentially expressed miRNAs were identified, and their predicted targets underwent Gene Ontology and KEGG pathway enrichment analyses. Serum proteomics by data-independent acquisition LC–MS/MS was integrated with miRNA data to construct potential miRNA–protein interaction networks. Distinct miRNA profiles were observed across the three bodily fluids, with serum showing the most abundant miRNAs and saliva the lowest. Thirteen, three, and six differentially expressed miRNAs were detected in serum, saliva, and vaginal mucus, respectively. Enrichment analysis implicated apoptosis, Wnt signaling, autophagy, and cellular senescence. Integrated analysis revealed 59 upregulated serum proteins targeted by dysregulated miRNAs, including WNK2, CD44, USP15, GNAI3, HUWE1, and NRAS. ROC analysis suggested that serum miR-200a-3p and miR-200b-3p, may have potential utility as noninvasive biomarkers for the diagnosis and monitoring of endometriosis, pending further validation. - Source: PubMed
Publication date: 2026/01/25
Lyu ShiqingLi QiutongGu ZhiyueYan HailanTang XinyueDai YiLi XiaoyanWu YushiZhang ChenyuXu YiyaoLi YuanyuanHu YaoWong Wing HingYu YanqinLu ShenBischoff Farideh ZLeng JinhuaShi Jinghua - Bovine spastic syndrome, known as Crampy, is a neuromuscular disorder in cattle. Affected cattle, 2 yr or older, suffer from involuntary muscle spasms in their hind limbs, leading to discomfort and reduced mobility. This often results in early culling from the herd, causing substantial financial loss for producers. Given the welfare implications and economic burden associated with Crampy, it is crucial to identify effective strategies to mitigate its occurrence. In this study, we assessed the feasibility of genetic selection to reduce Crampy by estimating variance components, evaluating the effect of incorporating genomic information, investigating Crampy's relationship with other economically important traits, and identifying genomic regions associated with Crampy in Canadian Holstein dairy cattle. A dataset comprising 54,826 animals, including 1,952 cases of Crampy, from 678 Canadian dairy herds, was provided by Lactanet Canada (Guelph, ON, Canada). Of these animals, 22,408 (including 408 with Crampy) were genotyped. Both threshold and linear models were used to estimate variance components, with observed scale h estimates ranging from 0.057 to 0.085. The inclusion of genomic data significantly increased the reliability of breeding values by 5% to 17%. Through a GWAS using GCTA software, a total of 41 significant SNPs were found to be significantly associated with Crampy. Functional analysis revealed 44 genes, among which we have highlighted the genes WNK2 (BTA8), DTNBP1 (BTA23), and ADK (BTA28), which have been associated with ion transport, muscle function, and neuron signaling, respectively. Enriched colocated QTL annotations linked to ketosis, muscle calcium content, and muscle zinc content were also identified, highlighting the role of metabolic processes and mineral homeostasis in muscle function. Breeding value correlations between Crampy and production, health, longevity, and type traits, and the selection indices were moderately low but favorable, indicating that current breeding strategies may indirectly select against Crampy. These findings highlight genomic selection as a viable strategy to mitigate Crampy in Canadian dairy herds, emphasizing the need for continued phenotyping for this disorder and optimization of breeding practices to improve animal welfare and sustainability. - Source: PubMed
Publication date: 2025/10/10
Condello GabriellaSchenkel Flavio SHermisdorff Isis CLynch ColinRochus Christina MVan Doormaal Brian JMiglior FilippoBaes Christine F - Chondrocytes of the synovial joint sense and respond to changes in osmolarity to maintain joint homeostasis. We hypothesised that an abnormal response to osmotic stress is a contributing factor to loss of joint homeostasis and the development of osteoarthritis (OA). Our goal was to identify whether genetic variants affecting the response to osmotic stress were associated with susceptibility to OA. - Source: PubMed
Publication date: 2025/07/01
Veerabhadraiah Shivakumar RMatheson Derek JHoneggar MatthewAslor CollinZelada Antonio CStubben ChrisStoddard Gregory JKazmers Nikolas HGrunwald David JJurynec Michael J