Ask about this productRelated genes to: WNT3 antibody
- Gene:
- WNT3 NIH gene
- Name:
- Wnt family member 3
- Previous symbol:
- INT4
- Synonyms:
- MGC131950, MGC138321, MGC138323
- Chromosome:
- 17q21.31-q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-30
- Date modifiied:
- 2018-02-13
Related products to: WNT3 antibody
Related articles to: WNT3 antibody
- Breast cancer survivors (BCS) often exhibit persistent metabolic and hepatic disturbances after cancer treatment; however, cardiorespiratory fitness's (CRF) underlying molecular signatures and associations of CRF with metabolic and hepatic health remain insufficiently understood. We examined whether circulating metabolic markers and WNT1-inducible signaling pathway proteins (WISPs) differ between BCS and matched controls, as well as whether CRF relates to metabolic and hepatic risk within BCS. To this end, 40 BCS and 40 age- and weight-matched healthy controls underwent assessment vis-à-vis anthropometrics, fasting metabolic biomarkers, liver enzymes, and fatty liver index (FLI). CRF was estimated using a standardized step test. Circulating WISP-1 and WISP-3 were quantified by enzyme-linked immunosorbent assays. Compared with controls, BCS exhibited lower CRF and higher body fat percentage, fasting insulin, insulin resistance, liver enzyme levels, and FLI. Circulating WISP-1 was higher in BCS, even after adjusting for age, menopausal status, and body fat percentage (adjusted ratio 1.23, 95% CI 1.01-1.52; p < 0.05). Differences in insulin resistance and hepatic risk were attenuated after adjustment, while the between-group difference in WISP-3 was not significant after covariate adjustment. Among BCS, higher CRF was associated with lower insulin resistance, reduced hepatic risk, and lower prevalence of FLI > 30 (57.9% 20.0%, p < 0.05) and metabolic syndrome (57.9% 5.0%, p < 0.001), while WISP concentrations did not differ by CRF. BCS demonstrated persistent metabolic vulnerability and elevated circulating WISP-1, regardless of adiposity and menopausal status. The findings show that higher CRF was associated with lower metabolic and hepatic risks. - Source: PubMed
Publication date: 2026/07/22
Min JiheeOh MinsukChang EunhaChoi Ji YeongAn Ki-YongKong In Deok - Death-associated protein kinase 1 (DAPK1), a Ca²+/calmodulin-regulated serine/threonine kinase, plays a pivotal role in epidermal homeostasis, tissue repair, and cutaneous wound healing. However, its role in oral mucosal repair remains unclear. In this study, we established a global knockout mouse model to create 1.5-mm circular palatal wounds in mice aged 8 to 12 wk. Our results demonstrated that DAPK1 deficiency significantly accelerated oral wound closure. In vitro experiments further confirmed that DAPK1 modulates the proliferation and migration of human oral keratinocytes. Mechanistic investigations through transcriptome sequencing revealed activation of the Wnt signaling pathway in knockout mice following injury, characterized by pronounced upregulation of , , and , alongside downregulation of innate immune mediators, including , , , , and . These findings suggest that loss of DAPK1 enhances epithelial proliferation and migration while attenuating local inflammation. Furthermore, we developed a novel microneedle patch for drug delivery, consisting of GelMA tips encapsulating the DAPK1 inhibitor (HS-38) and a hyaluronic acid substrate. This system facilitated efficient mucosal penetration and localized delivery. Application of the microneedle patch significantly improved wound healing in both normal and diabetic mouse models. Collectively, these findings uncover a previously unrecognized role of DAPK1 in oral mucosal repair and highlight its potential as a molecular target to accelerate wound healing. - Source: PubMed
Publication date: 2026/07/17
Li YHu MYin HCao YWu JYang MZhang XZhou JFang XLuo JHu MLi DLiu D - ObjectiveTo investigate the association between Wnt signaling pathway genes and non-syndromic orofacial cleft (NSOC) in the Han Chinese population.DesignBased on a previously published genome-wide association study (GWAS), we performed a discovery phase analysis on 635 QC-passed SNPs (out of 7054 initially extracted from 59 Wnt pathway genes). Significant loci were then validated in an independent replication cohort.SettingA specialized craniofacial surgery center within a tertiary care institution.Patients/ParticipantsIn the discovery phase, we extracted the genotype data of 2512 NSOC cases and 2255 controls from two previous published GWASs. The independent replication cohort included 2724 patients with NSOC and 1263 healthy controls, all of Han Chinese descent.InterventionsNo clinical interventions were applied; the study involved genetic data analysis only.Main Outcome MeasuresSNPs associated with NSOC and its subtypes were identified through allelic and genotypic association analyses, with odds ratios (ORs), 95% confidence intervals (CIs), and -values calculated.ResultsIn the independent replication cohort, rs4821611 in was significantly associated with NSOC ( = 5.8 × 10, OR = 0.77, 95% CI: 0.70-0.85), NSCL/P ( = 4.4 × 10, OR = 0.68, 95%CI: 0.61-0.77), and NSCLO ( = 3.27 × 10, OR = 0.6, 95% CI: 0.53-0.68). Genotypic analysis confirmed these associations. rs757190 in was also associated with NSCLP ( = 0.00056, OR = 0.78, 95% CI: 0.67-0.90).Conclusionsrs4821611 in and rs757190 in are associated with NSOC and its subtypes in the Han Chinese population, supporting a role for Wnt signaling in cleft pathogenesis. - Source: PubMed
Publication date: 2026/07/07
Jia SixuanYao MeilinBa WenqiZhang SidiYou YueDuan ShijunShi BingJia Zhonglin - To observe the effect of moxibustion at the governor vessel on lncRNA-RP4/miR-939-5p and Bnip3 in APP/PS1 double transgenic mice mediated by Wnt/β-catenin pathway, and to explore the mechanism of moxibustion in the treatment of Alzheimer's disease (AD). - Source: PubMed
Publication date: 2025/08/19
Zhou BingyuanZhu CaifengChen XiaoyuLi JingGao DahongWu AnqiTao LiYuan XinyiYang GaoshangChen XiyangXie MiaomiaoCheng LeWang Xuewei - Hyperactivating mutations in guanylyl cyclase C (GC-C) are monogenic causes of early-onset inflammatory bowel disease, familial diarrheal syndrome, and congenital secretory diarrhea. The mechanisms linking elevated cGMP levels to immune imbalance remain poorly defined. Here, using a preclinical model of a disease-associated GC-C mutation, we observe pleiotropic alterations in the small intestinal epithelium. Transcriptomic and functional analyses revealed impaired Paneth and goblet cell differentiation, compromised barrier integrity, heightened epithelial permeability, and increased proinflammatory cytokine levels. Intestinal organoids from mutant mice exhibited amplified cGMP responses to GC-C ligands and defects in secretory lineage specification, confirming cell-autonomous mechanisms. Strikingly, oral zinc administration suppressed aberrant GC-C activity, normalized cGMP levels, and restored barrier function. These findings highlight the central role of epithelial cGMP signaling in coordinating barrier integrity and immune-epithelial interactions and identify zinc as a tractable therapeutic strategy for GC-C-mediated intestinal disorders. Activating mutations in , which encodes the receptor guanylyl cyclase C (GC-C), cause early-onset diarrheal disease and gastrointestinal inflammation. Knock-in mice carrying a familial diarrheal syndrome mutation exhibited impaired gut barrier function. Mutant organoids showed defective secretory lineage specification associated with reduced Wnt3 expression. Zinc administration, which lowers epithelial cGMP levels by inhibiting GC-C, reversed most pathological changes in both mice and organoids. - Source: PubMed
Publication date: 2026/06/24
Bose AvipsaBopanna YashikaShetty PallaviSharma KriticaMathew John Kandam KulathuMishra VishwasBannerjee SanghitaRamani HariniPulimood Anna BBhat RamrayShenoy Avinash RVisweswariah Sandhya S