Tnfrsf11b
- Known as:
- Tnfrsf11b
- Catalog number:
- 043095A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Tnfrsf11b
Related genes to: Tnfrsf11b
- Gene:
- TNFRSF11B NIH gene
- Name:
- TNF receptor superfamily member 11b
- Previous symbol:
- OPG
- Synonyms:
- OCIF, TR1
- Chromosome:
- 8q24.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-05
- Date modifiied:
- 2016-10-05
Related products to: Tnfrsf11b
Related articles to: Tnfrsf11b
- Natto, a well-known fermented soybean product beneficial for bone health, remains unclear in its mechanism. - Source: PubMed
Publication date: 2026/06/14
Zhang BimiSun MubaiLiu YongfuPan TongZhang XuecongHe YuguangGan XuetongLi DaMiao XinyuLuo ZhengyangNiu HonghongHua MeiWang Jinghui - Despite advances in emerging therapies, colorectal cancer (CRC) incidence continues to rise and clinical outcomes remain suboptimal, highlighting the need for improved management strategies. One potential therapeutic target is osteoprotegerin (OPG), a glycoprotein which exhibits context-dependent functions by interacting with both Receptor Activator of Nuclear Factor Kappa-B Ligand (RANKL) to produce anti-resorption effects and TNF-related apoptosis inducing ligand (TRAIL) to promote cell survival, potentially modulating key hallmarks of CRC progression. However, its translational potential remains underexplored. - Source: PubMed
Publication date: 2026/06/16
Ng Chester Yan JieLyu ZipanLi MengXu LinWang NingZhong Linda L D - The selective EP4 receptor (PTGER4) agonist KMN-159 stimulates osteoblast function and may support applications in dental bone tissue regeneration and tissue engineering. The goal of this study was to further validate stimulation of osteogenic differentiation ex vivo and in vivo by KMN-159. We tested KMN-159 in cultured human bone marrow-derived mesenchymal stem/stromal cells (BM-MSCs) and rat BM-MSCs grown in a three-dimensional deproteinized bone explant culture model. The effects of KMN-159 treatment in vivo were also investigated in two different alveolar bone repair models (i.e., male rat tooth socket model with and without a dental implant), as well as in a pilot study with a dental repair model in which human implants were insert into the mandibles of male minipigs. Our results show that KMN-159 promotes osteogenic differentiation of human BM-MSCs, (e.g., ALPL enzyme and mineralization) and the temporal expression of osteoblast markers (e.g., RUNX2, SP7, BMP2, TNFRSF11B) and extracellular matrix (ECM) proteins (e.g., BGLAP). KMN-159 also stimulates osteogenesis in rat BM-MSCs in bone-derived 3D scaffolds by accelerating proliferation and modulating expression of osteoblast phenotype markers. In the in vivo studies of bone repair KMN-159 increases bone volume in the tooth socket or around the coronal aspect of the implant in the rat maxillary extraction models. Similar results were obtained in the porcine dental implant repair model. We conclude that KMN-159 is a viable pharmacotherapeutic candidate to promote bone mass accrual or to support bone tissue engineering in dental, craniofacial and skeletal applications. - Source: PubMed
Publication date: 2026/06/17
Owen Thomas ARzeczycki PhillipLeguizamon Natalia Da PonteJin QimingPatel ChandniWei ShanqiaoBarrett Stephen Dvan Wijnen Andre JMorano María Inés - In this cohort, we explored the DNA methylation changes of 3 genes of the canonical Wnt/β-catenin and RANKL/OPG pathways related to bone homeostasis in cord blood at birth. Those mothers with poor sleep quality in the first trimester of pregnancy had 5.9 times higher odds of complete OPG methylation compared to those with good sleep (adjusted OR = 5.9; 95% CI 1.04-33.0; p = 0.045). Maternal lifestyle factors during pregnancy can influence fetal development through epigenetic mechanisms, potentially affecting neonatal skeletal programming and long-term bone health. Sleep quality is an important, modifiable maternal factor, but its role in shaping epigenetic regulation of bone development remains unclear. We aimed to investigate the association between maternal sleep quality during pregnancy and DNA methylation of key genes of the canonical Wnt/β-catenin signaling pathway, Wnt Family Member 10B (WNT10B), β-catenin (CTNNB1), and osteoprotegerin (OPG or TNFRSF11B) in the offspring's cord blood samples at birth. A total of 300 pregnant women were recruited as a sub-study of the PERSIAN Birth Cohort-Isfahan. Maternal sleep patterns were assessed using the Pittsburgh Sleep Quality Index (PSQI). Methylation at cytosine-guanine (CpG) dinucleotide sites within the promoters of WNT10B, β-catenin, and OPG was quantified in offspring's cord blood at birth, and associations with maternal sleep quality across all trimesters were assessed. Poor sleep quality in the first trimester was significantly associated with increased OPG methylation (adjusted OR = 1.40, 95% CI 1.05-1.8, p = 0.023). Mothers with poor sleep quality (PSQI ≥ 5) in the first trimester had 5.9 times higher odds of complete OPG methylation compared to those with good sleep quality (adjusted OR = 5.9, 95% CI 1.04-33.0, p = 0.045). However, associations with WNT10B and β-catenin were not statistically significant. Maternal sleep quality during early gestation may influence the DNA methylation and epigenetic programming of bone-related genes in neonatal cord blood, emphasizing the importance of maternal lifestyle as a modifiable factor shaping early-life bone health. - Source: PubMed
Publication date: 2026/05/28
Baradaran Mahdavi SadeghNiazmand AnooshaJavadirad Seyed MortezaDaniali Seyede ShahrbanooMozafarian NafisehRoudashti ShekoufehHeidari-Beni MotaharRafieian MahsaBemanalizadeh MaryamPoursafa ParnianAzimian Zavareh VajiheFeizi AwatSalehi RasoulKelishadi Roya - Poor bone quality in osteoporotic patients remains a major challenge for achieving predictable osseointegration. This study serves as a mechanistic complement to previously reported structural data, aiming to investigate the molecular pathways underlying the synergy between nanostructured surfaces and autologous blood concentrates in compromised bone. Ninety-six Wistar rats were divided into healthy (SHAM) and osteoporotic (OVX) groups. Implants with nanostructured hydroxyapatite (NanoHA) or dual acid-etched (DAE) surfaces were installed in the tibiae, associated or not with leukocyte- and platelet-rich fibrin (). Gene expression (RT-qPCR) for , , , , , and was assessed at 7 and 30 days. In compromised systemic conditions (OVX), the NanoHA + association promoted a robust "molecular rescue" of bone metabolism. At 30 days, this synergistic group exhibited a significant upregulation of (mean: 11.69 ± 1.65) and (mean: 4.49 ± 0.82) compared to DAE controls ( < 0.05). Crucially, the therapy orchestrated a protective remodeling environment by significantly inducing expression (5.50 ± 0.88), effectively balancing the / ratio. Late-stage maturation markers ( and ) were also significantly elevated, effectively mimicking healthy physiological levels observed in the SHAM group. NanoHA biofunctionalization, synergistically with L-PRF, triggers a transcriptional reprogramming of the peri-implant microenvironment, mitigating the catabolic effects of estrogen deficiency. These findings provide a biological foundation for enhanced clinical predictability in high-risk patients, suggesting that local interfacial modifications can overcome systemic bone compromise. - Source: PubMed
Publication date: 2026/05/17
Barbosa Ana Carolina LoyolaJúnior José Augusto Gabarrada Silva Lilian Eslaine Costa MendesNóbrega FernandoBergamo Edmara Tatiely PedrosoGhiraldini BrunaE Pessoa Roberto SalesMessora Michel ReisSouza Sergio Scombatti de