Ask about this productRelated genes to: WNK1 antibody
- Gene:
- WNK1 NIH gene
- Name:
- WNK lysine deficient protein kinase 1
- Previous symbol:
- PRKWNK1, HSN2
- Synonyms:
- HSAN2, PPP1R167
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-06
- Date modifiied:
- 2019-04-23
Related products to: WNK1 antibody
Related articles to: WNK1 antibody
- Maintaining constant cellular osmolality is essential for physiological function in terrestrial animals. However, the molecular identity of the brain sensor(s) that detect extracellular hypertonicity and trigger arginine vasopressin (AVP) release has remained elusive. Early hypotheses emphasized the involvement of membrane mechanosensitive channels. More recent studies using purified proteins and heterologous expression systems have revealed that intracellular with-no-lysine (K) kinases (WNKs) possess intrinsic osmosensitivity. This review highlights emerging insights into how WNK1 senses environmental changes and regulates AVP secretion, thereby contributing to the maintenance of systemic water homeostasis. - Source: PubMed
Publication date: 2026/07/17
Jin XinAmir MohammadXie JianHuang Chou-Long - Colorectal cancer (CRC) progression is strongly influenced by interactions between tumor cells and the collagen-rich extracellular matrix. Discoidin domain receptor 1 (DDR1), a collagen-activated receptor tyrosine kinase, has been associated with poor prognosis in several epithelial malignancies, including CRC. However, the mechanisms by which DDR1 contributes to metastatic initiation remain incompletely understood. Here, we investigated the role of DDR1 in regulating CRC cell migration and invasion within type I collagen-rich microenvironments. DDR1 overexpression in low-invasive HT-29 cells was sufficient to enhance collective spheroid migration on collagen. Conversely, pharmacological inhibition or genetic silencing of DDR1 in highly invasive HCT-116 cells significantly impaired two-dimensional and three-dimensional migration as well as invasion within fibrillar collagen matrices. Mechanistically, DDR1 inactivation restored epithelial features, as evidenced by increased membrane localization of E-cadherin, decreased N-cadherin expression and reduced MT1-MMP expression. These findings indicate that DDR1 promotes invasion through coordinated regulation of epithelial adhesion and localized collagen remodeling rather than global extracellular matrix degradation. Phosphoproteomic profiling further suggested that DDR1 activates a non-canonical pro-migratory signaling network independent of AKT and Wnt/β-catenin pathways, involving modulation of GSK-3, WNK1, and RSK signaling. Collectively, our results identify DDR1 as a critical regulator of collagen-dependent migration and invasion in CRC and highlight its kinase activity as a potential therapeutic target to limit metastatic progression. - Source: PubMed
Publication date: 2026/07/16
Roumieux MathildeCollin GuillaumeTerryn ChristineVan Gulick LaurenceMorjani HamidHachet CathySchneider ChristopheJaisson StéphaneDuca LaurentDedieu StéphaneBennasroune AmarAppert-Collin Aline - The 17th Annual Frontiers in Cancer Science (FCS) conference (2025) highlighted the convergence of multiomics, computational biology, and ancestry-specific genomics to advance proactive cancer care. Key insights included the role of epigenetic plasticity in maintaining tumor-propagating states and the identification of metabolic vulnerabilities, such as the WNK1-mTORC1 axis in leukemia and MAF-driven glutamine metabolism in myeloma. The meeting underscored the systemic nature of cancer, detailing how "cancer-educated" neutrophils prime premetastatic niches and how spatial exclusion mechanisms hinder immunotherapy. Breakthroughs in therapeutic engineering were showcased, including CD7-directed chimeric antigen receptor T cells and irreversible KRASG12C inhibitors. A critical focus remained on precision oncology for diverse populations, advocating for ancestry-aware datasets and long-read sequencing to address genomic disparities in Asian cohorts. Furthermore, the integration of artificial intelligence-driven "fragmentomics" and machine learning offers new pathways for early detection and tracking disease lethality. Collectively, FCS 2025 demonstrated that the future of oncology lies in integrating high-resolution disease models with robust data science to transition from reactive treatment to personalized, interceptive management. - Source: PubMed
Huang DachuanTee Wee WeiDe Mel SanjayItahana KojiSabapathy KanagaRamadan KristijanTaneja ReshmaLe Minh GiangOng Derrick Sek TongYeow Zhong YiOng S TiongZhou YilongKhong AnthonyLee Soo-ChinLucky Sasidharan SwarnalathaTam Wai LeongIyer N GopalakrishnaOng Choon Kiat - Type 4 renal tubular acidosis (RTA) is a common disorder characterized by hyperkalemic non-anion gap metabolic acidosis. Although type 4 RTA is generally attributed to impaired renal ammoniagenesis induced by hyperkalemia, whether defects in distal nephron acidification contribute to its pathophysiology remains unclear. Here, we investigated alterations in distal nephron acidification machinery in Kelch-like 3 knock-in (KLHL3-KI) mice, a genetically engineered model of pseudohypoaldosteronism type II. KLHL3-KI mice exhibited hyperkalemia, hyperchloremia, and reduced serum bicarbonate levels, consistent with type 4 RTA. Phosphoenolpyruvate carboxykinase (PEPCK), a key enzyme involved in proximal tubular ammoniagenesis, was significantly reduced in KLHL3-KI mice as compared with wild-type mice. In addition, ATP6V1B1, a subunit of the vacuolar H-ATPase selectively expressed in intercalated cells, was significantly decreased in membrane fraction. Renal medullary expression of Rh C glycoprotein (RHCG), a major ammonia transporter in the distal nephron, was also reduced. To determine whether these changes were secondary to hyperkalemia, KLHL3-KI mice were fed a low-K diet. Correction of hyperkalemia with a low-K diet significantly increased RHCG abundance, whereas ATP6V1B1 levels remained unchanged. By immunostaining, we found that WNK1 bodies were detected in a subset of ATP6V1B1-positive cells. In sum, these findings demonstrate that distal nephron acidification pathways are dysregulated in KLHL3-KI mice. Whereas RHCG downregulation appears to be potassium-dependent, ATP6V1B1 reduction persists despite correction of hyperkalemia, suggesting the involvement of potassium-independent mechanisms. Our findings raise the possibility that dysregulated KLHL3 signaling contributes to impaired distal nephron acidification in type 4 RTA, which merits further investigation. - Source: PubMed
Publication date: 2026/06/24
Tomomitsu YoshihiroIshizawa KenichiKuribayashi-Okuma EmikoShibata Shigeru - The With-No-Lysine (WNK) kinase family plays critical roles in cellular signaling, yet its significance in acute myeloid leukemia (AML) remains unclear. - Source: PubMed
Publication date: 2026/06/05
Chen FangliWang YuanqinFu ZhenChang LiJiang XueweiZhang ZhizhiLi ChongyangLiu LigenYang Li