Ask about this productRelated genes to: WNT2B Blocking Peptide
- Gene:
- WNT2B NIH gene
- Name:
- Wnt family member 2B
- Previous symbol:
- WNT13
- Synonyms:
- XWNT2
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-05
- Date modifiied:
- 2016-10-05
Related products to: WNT2B Blocking Peptide
Related articles to: WNT2B Blocking Peptide
- Regulatory T cells (Tregs) are essential for maintaining immune homeostasis by suppressing excessive activation of effector T cells. Although several mechanisms of Treg-mediated suppression have been described, the molecular signals that contribute to this regulation remain incompletely understood. WNT signaling, best known for its roles in development and tissue homeostasis, has recently emerged as an important regulator of immune function, but its contribution to Treg-mediated immune suppression is largely unknown. Here, we show that Tregs preferentially express multiple canonical WNT ligands, including WNT2B, WNT3, WNT7B, and WNT10B, compared with conventional CD4 T cells. These WNT proteins were detected intracellularly in Tregs, and WNT2B and WNT3 were actively secreted into culture supernatants. Conventional CD4 T cells expressed Frizzled receptors capable of sensing these ligands. Pharmacological inhibition of canonical WNT signaling using the antagonist mDKK-1 enhanced CD4 T cell activation and proliferation and increased pro-inflammatory cytokine expression, while anti-inflammatory IL-10 remained unchanged. Together, these findings identify Tregs as a source of canonical WNT ligands and suggest that Treg-derived WNT signaling contributes to the suppression of effector CD4 T cell responses. This work reveals a previously underappreciated pathway through which Tregs regulate immune activity and identifies WNT signaling as a potential target for modulating inflammatory immune responses. - Source: PubMed
Publication date: 2026/04/14
Singh Parihar KashishNiemeier Margaret RIfergan Igal - Dentine formation constitutes a physiological process precisely regulated by signal transduction modules governing odontoblast differentiation and mineralisation. First, by constructing a single-cell transcriptional landscape of odontogenic tissue, we defined EFNB2+ mesenchymal cells as a primary progenitor cluster, marking the origin of the odontogenic lineage. Integrating CellRank-based fate mapping and SCENIC-based regulon specificity analysis, we identified signal transducer and activator of transcription 3 (STAT3) as a pivotal transcriptional regulator of the odontoblast lineage. Subsequently, in silico perturbations using CellOracle predicted that STAT3 ablation disrupted the developmental vector field, redirecting the fate of mesenchymal precursors away from the odontoblast lineage. To substantiate these bioinformatic predictions, functional validation using shRNA-mediated silencing and pharmacological modulation demonstrated that STAT3 was essential for the proliferation and differentiation capacity of dental mesenchymal cells. Furthermore, we generated conditional knockout mice targeting Stat3 in Osterix-expressing odontoblast progenitors, which consequently exhibited significant dentine dysplasia. Mechanistically, RNA-seq and chromatin immunoprecipitation (ChIP) assays revealed that STAT3 directly bound to the WNT2B promoter, transcriptionally activating the Wnt/β-catenin signalling pathway in dental mesenchymal cells. Overexpression of WNT2B partially rescued the odontogenic defects induced by STAT3 inactivation. This 'prediction to verification' study establishes STAT3 as a critical regulator of dentinogenesis and provides potential therapeutic targets for the treatment of dentine developmental disorders and the advancement of dentine regeneration. - Source: PubMed
Publication date: 2026/04/15
Zhu YanfeiXu HongyuanZhang ZijianSun SiyuanHuang ZihanGao XinPan HouwenHuang XiangruLiu YuanqiWang XinyuJia HanbinDai QinggangJiang Lingyong - Adenoid cystic carcinoma (ACC) is a biphasic malignant tumor characterized by myoepithelial and luminal differentiation. ACC can undergo high-grade transformation (HGT), presenting poorly differentiated features. - Source: PubMed
Publication date: 2026/04/05
Yuan WeiJiang XueLi Dongmei - Xerostomia, the subjective sensation of dry mouth, is a debilitating consequence of head and neck radiotherapy and autoimmune disorders such as Sjögren’s syndrome. It severely impairs oral health and quality of life by promoting mucosal ulceration, infection, malnutrition, and speech difficulties, yet effective regenerative treatments remain limited. Macrophages have recently emerged as critical regulators of salivary gland repair through their roles in coordinating inflammation, fibrosis, and epithelial regeneration; however, the molecular mechanisms governing macrophage activation and function in the injured salivary gland remain poorly defined. The Wnt/β-catenin signalling pathway is a key regulator of inflammation and tissue homeostasis across multiple organs, but its role in salivary gland macrophages has not been well characterised. Here, we investigated canonical Wnt/β-catenin signalling following murine submandibular gland injury induced by main excretory duct ligation, with deligation used in selected experiments to model repair. Using ; reporter mice, we observed an increase in Axin2⁺ cells and substantial recruitment of F4/80⁺ macrophages exhibiting active Wnt/β-catenin signalling within the injured, ligated gland. qPCR-based gene expression analysis revealed increased expression of , , and several Wnt genes, including and , at days 3 and 6 post-injury, and identified Wnt2 and Wnt2b as macrophage-secreted ligands. Notably, despite the injury-associated increase in Wnt/β-catenin signalling, Axin2⁺ cells did not give rise to acinar cells following deligation. Finally, conditional depletion of () using ; and ; mice increased the number of CD206⁺ macrophages and reduced fibrosis, indicating a potential association between Wnt signalling, macrophage polarisation, and fibrotic repair. Together, these findings identify Wnt/β-catenin signalling as a regulator of macrophage phenotype and tissue repair in the injured salivary gland, suggesting that targeted modulation of Wnt activity may promote regeneration and enhance functional recovery. - Source: PubMed
Publication date: 2026/03/11
Ahmed ArazSachdeva SuveerWhawell SimonMiletich Isabelle - The mechanism underlying retinal spheroid layer formation was investigated using Rax::GFP-positive retinal progenitor cells from human embryonic stem cell-derived retinal organoids. Single-cell RNA sequencing suggested the earlier cell-cycle exit in non-layered spheroids, while well-layered spheroids retained longer proliferative property with transiently activated canonical WNT2B-FZD7 signaling followed by temporary expression of non-canonical WNT5A. Despite structural differences in vitro, however, both non-layered and well-layered retinal spheroids on differentiation day 60 developed a layer of photoreceptors after transplantation in a retinal degeneration rat model, resulting in synaptic and functional integration. Additionally, part of the Rax::GFP-positive cells differentiated into non-retinal lineages, including ciliary marginal zone-like, retinal pigment epithelium, and spinal cord-like tissues in vitro, reflecting the heterogeneity of RAX-positive cells. These findings suggest that canonical and non-canonical WNT signaling pathways sequentially orchestrate early retinal morphogenesis, whereas environmental factors within the host retina strongly drive the alignment and functional integration of graft photoreceptors. - Source: PubMed
Publication date: 2026/03/05
Iwama YasuakiMasuda TomohiroYoshimura MikaWatanabe MikiyaOhigashi YokoFriedlander MartinNishida KohjiTakahashi MasayoNikaido ItoshiMandai Michiko