Ask about this productRelated genes to: WNT16 Blocking Peptide
- Gene:
- WNT16 NIH gene
- Name:
- Wnt family member 16
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q31.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-20
- Date modifiied:
- 2016-10-05
Related products to: WNT16 Blocking Peptide
Related articles to: WNT16 Blocking Peptide
- Mechanical stimulation plays a crucial role in odontoblast differentiation. However, the underlying molecular mechanisms remain unclear. We have previously shown that hydrostatic pressure (HP) applied to stem cells from human exfoliated deciduous teeth (SHED) promotes odontoblast differentiation by translocating RUNX2 and increasing WNT16 expression through PIEZO1 signaling. In this study, we further explored the downstream signaling cascade linking PIEZO1 activation and odontoblast differentiation. HP stimulation increased the expression of odontoblast differentiation markers PANX3 and DSPP, as shown by qPCR, and enhanced Alizarin Red staining-results significantly suppressed by siRNA targeting either PIEZO1 or WNT16. RT-PCR analysis revealed that, among the two known human WNT16 isoforms, only WNT16b was expressed in SHED. qPCR demonstrated that HP-induced WNT16 expression was reduced by siPIEZO1 and further decreased by siRUNX2. Promoter analysis identified four RUNX2-binding sites within the upstream region of WNT16. A luciferase reporter assay using plasmids containing the WNT16 promoter showed that RUNX2 overexpression in HEK293 cells significantly increased luciferase activity. Moreover, HaloChIP assays with a HaloTag-RUNX2 expression vector confirmed RUNX2's binding to the WNT16 promoter. These findings suggest that PIEZO1-mediated mechanical stress promotes odontoblast differentiation through the RUNX2-dependent transcriptional activation of WNT16. - Source: PubMed
Publication date: 2026/04/01
Miyazaki AyaNarwidina AnrizandySugimoto AsunaKurogoushi RikaNakashima YumikoHashimoto NoboruYamamoto AkihitoIwamoto Tsutomu - Osteoporotic non-vertebral fractures are a major clinical burden, with cortical bone impairment being a key pathogenic factor often overlooked in traditional treatments. This review aims to synthesize current evidence on the role of Wnt16 (a non-canonical Wnt ligand) in regulating cortical bone and its potential as a therapeutic target for osteoporotic non-vertebral fractures. We systematically review literature on Wnt16 in senile, postmenopausal, and glucocorticoid-induced osteoporosis, focusing on its mechanisms of action: (1) regulating bone mineral density via genetic associations with GWAS-identified loci; (2) reducing cortical bone porosity and increasing thickness; (3) dual regulation of osteoblasts (via JNK/β-catenin pathways) and osteoclasts (via OPG-dependent/independent NF-κB pathways). Wnt16 has been shown to improve bone density and reduce non-vertebral fracture risk in preclinical models, though conflicting findings exist regarding its full compensation for glucocorticoid-induced bone loss. We conclude that Wnt16 is a promising target for non-vertebral fracture prevention, with Notum inhibitors emerging as potential therapeutic agents. This review provides a comprehensive framework for future clinical and translational research. - Source: PubMed
Publication date: 2026/03/09
Tianpeng ChenQishui XiaFo YangMingjun WuHaibo HuJiuchu JinXiaolin ShiGongtao Jiang - Bone mineral density (BMD) is a critical indicator of osteoporosis (OP). Utilizing the latest multi-omics quantitative trait loci (QTLs) data, we aim to identify novel candidates associated with heel BMD (hBMD). - Source: PubMed
Publication date: 2026/03/24
Yang XuenaLiu HuanXu KeHe DanCheng ShiqiangPan ChuyuLiu LiWei WenmingZhao BoyueHui JingniWen YanJia YumengCheng BolunXu PengZhang Feng - The wnt gene family encodes a group of highly conserved secreted glycoproteins that play essential roles in vertebrate development, including tissue patterning, cell differentiation, and gonadal regulation. However, the genomic organization, evolutionary dynamics, and functional roles of Wnt signaling components in flatfish remain poorly understood. In this study, we performed a comprehensive genome-wide identification, evolutionary characterization, expression profiling, and functional analysis of wnt genes in , a flatfish species exhibiting ZW/ZZ sex determination and temperature-induced sex reversal. A total of 20 wnt genes were identified and classified into 13 subfamilies, displaying conserved structural organization and phylogenetic relationships consistent with other teleosts. Chromosomal mapping revealed lineage-specific WNT clusters, including a unique wnt3-wnt7b-wnt5b-wnt16 block, as well as syntenic associations with reproduction-related genes (e.g., , , , , ), suggesting coordinated genomic regulation. Tissue transcriptome analysis demonstrated strong sex- and tissue-biased expression patterns, with predominantly expressed in ovaries and specifically upregulated in pseudo-male testes. Functional assays revealed that knockdown of or induced testis-specific genes (, ) and suppressed ovarian markers (, ), indicating antagonistic regulatory roles in gonadal fate determination. Promoter analysis identified as a selective repressor of , but not , providing a mechanistic basis for paralog divergence. Furthermore, pull-down combined with LC-MS/MS analysis showed that WNT5b interacts with proteins enriched in ribosome biogenesis and ubiquitin-mediated proteolysis, suggesting a role in translational regulation and protein turnover during spermatogenesis. Together, these findings establish WNT5 signaling-particularly -as a key driver of testicular development in and provide new insights into the molecular mechanisms underlying sex differentiation and sex reversal in flatfish. - Source: PubMed
Publication date: 2026/01/26
Li ZhengjieWang JunhaoLi ChaoZhu Ying - Osteoporosis is characterized by an imbalance in bone remodeling, resulting in bone loss and increased fracture risk. Inflammatory diseases, such as rheumatoid arthritis, are strongly associated with secondary osteoporosis due to inflammation-induced bone loss. Pro-inflammatory cytokines, particularly TNF-α, disrupt bone homeostasis by promoting osteoclastogenesis and inhibiting osteoblast function. The Wnt signaling pathway is essential for bone formation and is suppressed in inflammatory conditions. WNT16, an osteoblast-derived ligand, increases bone mass mainly by inhibiting osteoclast differentiation but has also been found to stimulate osteoblast activity. Here we demonstrate that TNF-α downregulates Wnt16 mRNA expression in primary osteoblasts, suggesting that inflammation may impair WNT16 expression and thereby reduce bone mass. To evaluate whether pharmacological or genetical elevation of WNT16 levels can mitigate inflammation-induced bone loss, we examined the effect of WNT16 in three mouse models of local and systemic inflammation. In a knee arthritis model, intra-articular delivery of WNT16 liposomes failed to prevent local bone loss. Similarly, although osteoblast-specific WNT16 overexpression increased the overall bone mass, it did not protect against either local calvarial bone loss or systemic bone loss induced by Toll-like receptor 2 (TLR2) activation. Furthermore, in a model of systemic inflammation induced by Staphylococcus aureus, WNT16 overexpression did not preserve vertebral trabecular bone, despite increased baseline bone mass. These findings demonstrate that WNT16, although increasing the overall bone mass, is insufficient to counteract inflammation-driven bone loss. - Source: PubMed
Publication date: 2026/01/31
Nilsson Karin HHenning PetraLagerquist Marie KWu JianyaoBally MartaLerner Ulf HGjertsson IngerOhlsson ClaesMovérare-Skrtic Sofia