Ask about this productRelated genes to: WNT10B antibody
- Gene:
- WNT10B NIH gene
- Name:
- Wnt family member 10B
- Previous symbol:
- -
- Synonyms:
- WNT-12, SHFM6
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-05
- Date modifiied:
- 2016-10-05
Related products to: WNT10B antibody
Related articles to: WNT10B antibody
- The cerebellum relies on Purkinje cells (PCs) to coordinate motor functions and maintain neural circuitry. Impaired PC dendritogenesis is linked to neurological disorders, yet intrinsic molecular mechanisms remain unclear. We demonstrate that postnatal deletion of Yin Yang 1 () in PCs disrupts dendrite and spine formation, impairs synaptic plasticity, and alters protein kinase C gamma (PKCγ) expression, leading to cerebellar ataxia and progressive atrophy. Mechanistically, YY1 transcriptionally activates wingless-type MMTV integration site family, member 10B (), which signals through Frizzled-4 (Fzd4) in PCs. downregulation mimics the dendritic defects seen in mutants, indicating its crucial role in dendrite growth and synaptic environment regulation. These changes result in defective synapse innervation. Our findings reveal that YY1 governs PC dendritogenesis and synaptogenesis via , while also modulating PKCγ and β-catenin signaling. The YY1-Wnt10b axis emerges as a critical pathway underlying YY1-associated cerebellar dysfunction. - Source: PubMed
Publication date: 2026/07/31
Lui Ying LamDong XiaonanLeung Thomas Chun NingLi Tsz HoChan Ting FungKwan Kin Ming - Distraction osteogenesis (DO) is a surgical technique used to repair skeletal defects by promoting bone and soft tissue regeneration. However, prolonged use of external fixators often causes complications such as infections and joint contractures. Neurotrophin-3 (NT-3) enhances osteoblast differentiation via bone morphogenetic protein-2 (BMP-2) and Akt signaling and may also modulate the Wnt/β-catenin pathway. In this study, we investigated the role of NT-3 in bone regeneration during DO. A DO model was established in 9-week-old male ICR mice, in which tibiae were osteotomized and stabilized with external fixators under anesthesia. After a 5-day latency period, distraction was performed at 0.2 mm every 12 hours for 8 days. RNA was extracted at defined time points post-osteotomy for quantitative polymerase chain reaction (qPCR) analysis, and NT-3 was administered post-distraction. Bone regeneration was evaluated by radiographic, histological, and biomechanical analyses. The effects of NT-3 and Dickkopf-1 were further examined in ST2 bone marrow-derived mesenchymal stem cells. NT-3 significantly enhanced bone formation, increased bone mineral density within the DO gap, and improved the mechanical stiffness of regenerated bone. Histological examination revealed earlier bone continuity and greater callus formation in the NT-3 group. Gene expression analysis demonstrated upregulation of Wnt/β-catenin pathway components, including Wnt10b, β-catenin, and low-density lipoprotein receptor-related protein 5 (LRP5). In ST2 cells, NT3 increased the expression of LRP5, LRP6, β-catenin, and Runx2, while cotreatment with Dickkopf1 abolished these effects. These findings suggest that NT-3 promotes bone regeneration during DO by activating the Wnt/β-catenin signaling pathway, highlighting its therapeutic potential to improve DO outcomes. - Source: PubMed
Wakasugi MasashiFujio MasahitoTsuboi MakotoChang QiBian HuitingLiu YuqingHibi Hideharu - Gastric precancerous lesions (GPLs) are a pivotal stage in the gastritis-gastric cancer sequence, and the absence of effective treatments presents a clinical challenge. Veratramine is a natural anti-inflammatory and analgesic steroid alkaloid; however, its effects on GPLs and the mechanisms have remained unexplored. This study investigated the effects of veratramine on GPLs using 1-Methyl-3-nitro-1-nitrosoguanidine (MNNG)-induced GES-1 cells and rat models, utilizing RNA-seq to elucidate the underlying mechanisms. In vitro, veratramine inhibited malignant cells (MC) proliferation, induced apoptosis, and triggered G0/G1 cell cycle arrest. It also suppressed epithelial-mesenchymal transition (EMT), migration, and invasion by upregulating E‑cadherin and downregulating Slug and vimentin. Transcriptomic and molecular docking analyses highlighted the Wnt/β-catenin pathway as a key target, regulated via DDX60, MUC1, APOL1, and MSH5. Veratramine reduced Wnt10B, β-catenin, and cyclin D1 expression and blocked β‑catenin nuclear translocation; these effects were reversed by the Wnt activator BML-284. In vivo, treatment with veratramine ameliorated the GPLs-induced pathological changes in rats. It restored body weight and preserved gastric mucosal integrity, as evidenced by intact glandular and cellular morphology, reduced hyperplasia, and attenuated intestinal metaplasia. These improvements were associated with a modulation of key molecular markers, specifically a decrease in the expression of N-cadherin, Wnt10B, and β-catenin, alongside an increase in E-cadherin expression in gastric tissues. These results collectively indicate that veratramine exerts its therapeutic effects against GPLs primarily by suppressing the Wnt/β-catenin signaling pathway. Taken together, our findings suggest that veratramine is a promising candidate small-molecule drug for the treatment of GPLs. - Source: PubMed
Publication date: 2026/07/30
Zhang PanSun XuelinLiu LongtengZhang YatongBo JiaqiHuang WenliNa YifanZhang JingyiQin XiaoyunLuo Qingfeng - Sarcoids are the most common cutaneous tumors in horses, representing up to 90% (35%-90%) of skin neoplasms. Mostly caused by Bovine Papillomavirus (BPVs) infections, sarcoids are highly resistant to therapy and prone to recurring, posing a significant threat to equine health. The aim of this study is to explore molecular pathogenetic mechanisms underlying the development of equine sarcoids, by applying transcriptomic approach. After testing samples for viral DNA, both mRNA and small RNA expression was analyzed via high-throughput Illumina sequencing comparing 12 sarcoids and 12 healthy skin samples as controls. Differentially expressed genes (DEGs), DE miRNAs (sarcoids vs. controls) and miRNA-DEG couples with opposite expression trends, were retrieved and subjected to a functional analysis. Over 6K DEGs emerged, 3620 down-regulated and 2415 up-regulated along with 145 DE miRNAs, 56 downregulated and 89 upregulated. Among the enriched biological processes for DEGs, some were related to growth factors production and collagen binding, cell migration and proliferation, tissue morphogenesis and inflammatory response. Interestingly, "Pathways in cancer" and "Hippo signaling pathway" were enriched KEGG pathways for the miRNA-DEG couples. Our data identified a great transcription discrepancy between sarcoid lesions and healthy skin with an overall enrichment for processes related to cellular transformation. RNA-seq sequencing depth allowed the search for candidate chimeric transcripts associated with viral integration events. Chimeric RNAs can influence gene regulation and may contribute to tumor growth and immune modulation. Via computational analysis we identified six fusion loci in tumor samples and in two sarcoid margins, with the most frequent event involving WNT10B and FKBP11. This fusion, detected in 6/10 sarcoids, is of particular interest since WNT10B activates the WNT/β-catenin cascade, while FKBP11 has been implicated in osteosarcoma progression. Although functional validation is ongoing, this represents the first report of chimeric transcripts in equine sarcoids, opening new perspectives on BPV-driven oncogenesis. - Source: PubMed
Publication date: 2026/06/19
Mecocci SamantaCapomaccio StefanoPorcellato IlariaDell'Anno FilippoRatto RobertaMechelli LucaDe Paolis LiviaFruscione FlorianaPasseri BenedettaGialletti RodolfoPepe MarcoGhelardi AlessandroRazzuoli ElisabettaCappelli Katia - The prevalence of osteoporosis is increasing worldwide as populations age, creating a growing clinical burden of fragility fractures and highlighting limitations of current antiresorptive therapies. Conventional agents such as bisphosphonates and denosumab effectively reduce fracture risk but suppress osteoclast number and activity indiscriminately, potentially impairing bone remodeling dynamics and silencing osteoclast-derived anabolic and angiogenic coupling signals. Recent advances have redefined osteoclasts as multifunctional cells that not only resorb bone but also orchestrate osteoblast differentiation and type H angiogenesis through factors such as PDGF-BB, S1P, Wnt10b, BMP6, and CTHRC1. These insights underscore the need for therapeutic strategies that temper pathological resorption while preserving beneficial coupling. This review integrates emerging molecular mechanisms regulating two key functions of osteoclasts, progenitor cell fusion and functional polarization, and evaluates their translational potential as selective antiresorptive targets. Fusion is driven by fusogen (DC-STAMP, OC-STAMP, Atp6v0d2, CD9, integrins), recognition systems (DC-STAMP, Siglec-15-sialylated TLR2), and alterations in membrane-cortical adhesion mediated by phosphatidylserine exposure, annexin A5, ERM, and BAR proteins. Osteoclast polarization relies on integrin αvβ3-Src-Pyk2 signaling, Rho-family GTPases. Recently, leucine-rich repeat kinase (LRRK1) has attracted attention as a factor that integrates both c-Src signaling and Rho-family GTPase signaling. Therapeutically, multiple modalities such as neutralizing antibodies against DC-STAMP/OC-STAMP, Siglec-15 inhibitors, small molecules such as E8431 (DC-STAMP antagonist) and C21 (Dock5 inhibitor), and LRRK1 inhibitors demonstrate the feasibility of selectively modulating fusion or polarization while maintaining osteoblast-coupling pathways. These strategies may complement conventional antiresorptives to provide safer, more physiologically balanced osteoporosis treatments. Collectively, emerging evidence positions osteoclast fusion and polarization as highly selective and clinically promising targets. A future therapeutic framework may integrate: (i) modest suppression of osteoclast number, (ii) targeted fusion inhibition to preserve preosteoclast-derived blood vessel formation, and (iii) polarization-directed modulation to reduce resorption while sustaining bone formation. - Source: PubMed
Publication date: 2026/06/05
Uehara ShunsukeNakamura MidoriKobayashi YasuhiroUdagawa Nobuyuki