Ask about this productRelated genes to: Wnt1 protein
- Gene:
- WNT1 NIH gene
- Name:
- Wnt family member 1
- Previous symbol:
- INT1
- Synonyms:
- -
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-18
Related products to: Wnt1 protein
Related articles to: Wnt1 protein
- Craniosynostosis is a debilitating congenital anomaly characterized by the premature fusion of cranial sutures in the skull, resulting from the abnormal fate specification of critical skeletal stem cells. This leads to disrupted craniofacial development and dysmorphology. As an alternative to invasive cranial vault remodeling surgery, we propose a tissue engineering approach to effectively restore the damaged or absent suture stem cell niche using a biomaterial capable of regioselective stem cell maintenance, marking a significant paradigm shift. By harnessing the role of biomaterial scaffold pore design to direct cell fate, we developed a "bone-suture-bone" design within a triphasic scaffold. We demonstrate that this unique scaffold design maintains stemness in a central region while promoting osteogenic differentiation in the surrounding areas, replicating the interfaces and function of the native suture. The scaffold's ability to reconstitute an engineered skeletal stem cell niche and facilitate the functional recovery of the craniosynostosis phenotype is validated in a caBmpr1a; Wnt1-Cre murine model of midline craniosynostosis, the most common nonsyndromic clinical presentation in humans. This work shows significant promise for improving patient outcomes through a rational tissue engineering strategy for reconstituting a native stem cell niche. - Source: PubMed
Publication date: 2026/05/28
Benton Swanson WDouglas LindseyWoodbury Seth MAlbright JacksonPan HaichunOmi-Sugihara MaikoEberle MirandaHerremans JakeNam Hwa KyungCavalcante Rafael CorreiaChen CoralMa Peter XHatch Nan EMishina Yuji - : Chronic Mild Stress (CMS) provokes neuroendocrine dysregulation and oxidative injury that compromise neuronal integrity and plasticity. Disruption of the canonical Wnt/β-catenin signaling pathway has been increasingly linked to stress-induced neurobiological dysfunction. Vitamin D3, a neuroactive hormone with antioxidant and immunomodulatory properties, may exert neuroprotection through modulation of this pathway and attenuation of oxidative damage. The study aims to investigate whether vitamin D3 mitigates CMS-induced alterations in Wnt/β-catenin signaling, oxidative stress markers, and oxidative DNA damage in male Wistar rats. : Thirty-two male Wistar rats were randomly allocated into four groups ( = 8/group): control, CMS only, CMS + vitamin D3 (1000 IU/kg), and CMS + vitamin D3 (10,000 IU/kg). Vitamin D3 was administered intramuscularly three times weekly for 28 days. Hippocampal mRNA expression of Wnt pathway components and brain-derived neurotrophic factor (BDNF) was quantified by RT-qPCR using the 2 method. Oxidative stress was evaluated by measuring malondialdehyde, glutathione, superoxide dismutase, and catalase, while DNA damage was assessed via 8-OHdG ELISA. : CMS significantly downregulated Wnt1, β-catenin, and Axin2 mRNA expression ( < 0.05) while markedly upregulating GSK-3β ( < 0.001). Expression of BDNF was also reduced ( < 0.05). Biochemically, CMS increased MDA and 8-OHdG levels (both < 0.001) and decreased glutathione ( < 0.001), superoxide dismutase, and catalase activities ( < 0.05). Vitamin D3 supplementation significantly reversed these transcriptional and biochemical alterations, restoring β-catenin signaling, improving antioxidant defenses, and reducing oxidative and genotoxic damage. : Vitamin D3 confers significant neuroprotection under chronic stress by modulating Wnt/β-catenin signaling and attenuating oxidative and DNA damage, thereby enhancing neuronal resilience to prolonged stress exposure. - Source: PubMed
Publication date: 2026/04/24
Alrashed May MTabassum HajeraAldisi DaraAlhussain Maha HArjumand SadiaAbulmeaty Mahmoud M A - Osteogenesis imperfecta (OI) is a genetically and clinically heterogeneous bone disorder, with more than 20 genes contributing to OI development. Previously, we identified c.620G > A (p.Arg207His) mutation among Chinese patients with autosomal recessive OI (AR-OI). This study aims at investigating the causative role of deficiency in OI and evaluate whether AAV-based gene therapy could ameliorate bone abnormalities. We generated and analyzed the Wnt1 rat model. The AAV9-Wnt1 virus was delivered via direct intraosseous injection into the femoral marrow cavity of the OI rats to evaluate its therapeutic potential. The homozygous Wnt1 rat recapitulated key features of AR-OI, including fractures, reduced bone mass, growth retardation, decreased survival rate, increased osteoclast numbers, diminished osteoblast function and mineralization capacity, compared with heterozygous and wild-type littermates. In vitro, overexpression in osteoblasts promoted osteoblast activity and bone mineralization. Furthermore, AAV9-Wnt1 treatment in OI rats resulted in significant recovery of bone density and mechanical strength, stimulation of osteoblast activity, suppression of osteoclast activity, and upregulation of Type I collagen expression. Our study demonstrates that c.620G > A (p.Arg207His) is pathogenic, and confirms that AAV-mediated Wnt1 gene therapy represents a promising strategy for treating OI caused by mutations. - Source: PubMed
Publication date: 2026/05/21
Li ShanChen XiuminCao YixuanHan MingchenGuan FeifeiRen XiuzhiMi HuanYang TaoLi MeiZhao Xiuli - Clinical studies suggested that antibiotics (ABx) administration might increase esophagogastric junction adenocarcinoma risk, but the underlying mechanisms remain unclear. We previously demonstrated that the administration of a high-fat diet (HFD) and acid bile salts (ABS) to K19-Wnt1/C2mE mice might promote the metabolic-driven tumor growth at the squamocolumnar junction (SCJ) cooperatively with gut dysbiosis. To clarify whether ABx-induced dysbiosis promotes the tumorigenesis, we evaluated the effects of HFD+ABS ± ABx treatment on tumor immune evasion in mice. In HFD+ABS+ABx-treated mice, SCJ tumor growth with increased tumor cell proliferation and infiltration of inflammatory cells positive for CD8, programmed cell death protein 1 and programmed cell death-ligand 1 (PD-L1) were observed along with apoptosis suppression. Protein expressions of interferon-gamma (IFN) and phosphorylated signal transducer and activator of transcription (p-STAT) 3 were upregulated in the tumors of the HFD+ABS+ABx group, whose p-STAT1 expression was equivalent to that of the control group. The mice exhibited insulin resistance and metabolic endotoxemia, and metagenomic analysis of their ileal excrement revealed dysbiosis with a decrease in butyrate-producing bacteria and bacterial butanoate metabolism activity. Moreover, IFN stimulation of human-derived NUGC-4 cells increased the protein expression of PD-L1, p-STAT1 and p-STAT3, all of which decreased in response to STAT inhibitors. Transfection with small interfering RNA targeting or did not attenuate PD-L1 induction, which was inhibited by the combined knockdown. Therefore, oral HFD+ABS+ABx administration to K19-Wnt1/C2mE mice may promote SCJ tumors through tumor immune evasion via IFN-STAT1/STAT3-PD-L1 signaling, along with metabolic endotoxemia. - Source: PubMed
Publication date: 2026/05/22
Ogasawara KoyaUno KanameTamahara ToruAsano NaokiSudo KoichiroKusano KeisukeTanabe MizukiKaise YumikoShindo TakafumiShimoyama YusukeKanno TakeshiKoike TomoyukiShimizu RitsukoMasamune Atsushi - Glutamate (Glu) accumulation-induced excitotoxicity is a major cause of retinal ganglion cell (RGC) death in glaucoma, and the role of ferroptosis, a novel form of cell death, is critical in this process. The aim of this study was to investigate the function and regulatory mechanisms of the lipid transport protein StarD7 in RGC ferroptosis. - Source: PubMed
Publication date: 2026/05/19
Zhang LiweiChu WenFeng XiaoxiaoPeng HuaGuo LiyunYang YabinKong Lei