RANKL antibody (Azide Free)
- Known as:
- RANKL (anti-) (Azide Free)
- Catalog number:
- 10r-8214
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RANKL antibody (Azide Free)
Related genes to: RANKL antibody (Azide Free)
- Gene:
- TNFSF11 NIH gene
- Name:
- TNF superfamily member 11
- Previous symbol:
- -
- Synonyms:
- TRANCE, RANKL, OPGL, ODF, CD254
- Chromosome:
- 13q14
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: RANKL antibody (Azide Free)
Related articles to: RANKL antibody (Azide Free)
- Excessive fluoride intake can lead to skeletal fluorosis, which is a global public health concern. In recent years, selenium-loaded chitosan nanoparticles (CS-SeNPs) have attracted considerable attention due to their high bioactivity and favourable adhesion to the intestinal mucosa, and have demonstrated significant potential in mitigating skeletal damage. Nevertheless, it remains unclear whether CS-SeNPs can improve fluoride-induced bone damage and what the underlying regulatory mechanisms are. In this study, we found that CS-SeNPs alleviated fluoride-induced intestinal barrier disruption and colonic microbiota dysbiosis by downregulating pro-inflammatory and toxin-producing bacteria Desulfovibrio and Bilophila. CS-SeNPs increased the levels of beneficial bacteria such as Lactobacillus and Blautia, suppressed the expression of tumor necrosis factor (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6), and reduced reactive oxygen species (ROS) and malondialdehyde (MDA) levels, thereby improving systemic chronic inflammation and oxidative damage. Furthermore, CS-SeNPs also enhanced the absorption of calcium and phosphorus by bone tissue and, via the gut-bone axis, inhibited the sustained activation of the bone osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL)/nuclear factor kappa-B (NF-κB) pathway, as well as the abnormal activation of osteoclasts, thereby restoring bone metabolic balance and effectively alleviating fluoride-induced bone damage. These findings reveal the unique mechanisms of CS-SeNPs in regulating bone resorption and bone formation, not only providing new insights into the interaction between CS-SeNPs and the intestinal microbiota, but also offering potential therapeutic strategies for alleviating fluoride-induced bone damage. - Source: PubMed
Publication date: 2026/06/23
Zhao HuiZhao TianruiWang JiaxinLi YuanyuanLi HaojieShi TongzhouZhao YangfeiZhang JianhaiWang JundongCheng XiaofangWang Jinming - Osteocytes are critical for bone development, and tightly regulate bone (re)modelling by directing the differentiation and activity of osteoblast and osteoclasts. Primary osteocyte isolation is challenging, therefore MLO-A5 and MLO-Y4 osteocyte-like cell lines have been instrumental in dissecting osteocytogenesis and bone mineralisation. Limited comparative analysis of these closely related in vitro models has been undertaken, therefore we used transcriptomic analysis to dissect their transcriptional similarities. Principal component analysis showed MLO-A5 and MLO-Y4 cells form distinct clusters, with 4451 differentially expressed genes. Known osteoblast markers (Alpl and Col1a1) and early osteocyte markers (Gja1, Pdpn, and Tnfsf11) predominated in MLO-A5 and MLO-Y4 cells, respectively. MLO-A5 cells expressed genes associated with extracellular matrix (re)modelling and mineralisation pathways, whilst MLO-Y4 cells were enriched with genes associated with cell signalling, consistent with MLO-A5 and MLO-Y4 cells representing different stages in osteocyte development. Androgens have anabolic effects on the bone, so their impact on the osteocyte transcriptome and osteocyte function was investigated. Surprisingly, androgen (Ar) and oestrogen receptor (Esr2) expression was significantly lower in MLO-A5 and MLO-Y4 cells compared to mouse tibiae. Treatment with androgen receptor ligands (R1881 and enzalutamide) had minimal effect on MLO-A5 or MLO-Y4 gene transcription (<20 differentially expressed genes) and treated cells showed a striking lack of differentially expressed osteoblast and osteocyte regulatory genes. This work provides a comprehensive understanding of these important in vitro osteocyte models and highlights the limitations of using MLO-A5 or MLO-Y4 cells to investigate the impact of sex hormones on osteocyte function in vitro. - Source: PubMed
Publication date: 2026/08/19
Wade Rachel LDunbar Donald RBergkvist Gurå TFarquharson ColinFraser Jennifer A - Orthodontic tooth movement (OTM) is regulated by alveolar bone remodeling through the receptor activator of nuclear factor kappa-B ligand (RANKL) and osteoprotegerin (OPG) axis. Clear plastic aligners (CPAs), available as thermoformed and direct-printed variants, differ in force delivery and material properties, influencing biomarker responses. - Source: PubMed
Publication date: 2026/08/07
Lakshmanan PoojaBaskaran ShivakumarAlamelu SwarnaBaskar Karthick - Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder characterized by the early development of pathological features associated with aging, ultimately leading to premature death. HGPS primarily affects tissues of mesenchymal origin, as evidenced by the clinical manifestations characteristic of this premature aging disorder, including, but not limited to, osteoporosis, muscle wasting, lipodystrophy, and cardiovascular disease. In this study, we used preclinical mouse models and both genetic and translational approaches to investigate whether an antiresorptive strategy, based on RANKL targeting, ameliorated the bone loss phenotype of progeroid mice. Here we show that osteocyte-derived RANKL deletion in the Zmpste24 mouse model of HGPS reverted bone loss in both long bones and vertebrae. These mice also exhibited increased grip strength and improved endurance capacity. Furthermore, Zmpste24 mice showed increased survival upon osteocyte-specific RANKL deletion. Notably, the use of a translational approach based on the administration of a neutralizing antibody against RANKL also restored bone mass, reduced muscle fibrosis, and extended the lifespan of Zmpste24 mice. Altogether, these findings support that targeting RANKL exerts a beneficial effect on both osseous and extra-osseous phenotypes of HGPS, suggesting the potential of this therapeutic approach to explore in the treatment of this disease. - Source: PubMed
Freitas-Rodríguez SandraValle-Cao AlejandraRodríguez FranciscoFernández-Sanjurjo ManuelFernández-García BenjamínLoredo VanessaFernández-García María TeresaFiuza-Luces CarmenLucia AlejandroLópez-Otín CarlosLópez-Soto AlejandroFolgueras Alicia R - To investigate the mechanisms underlying the bone-sparing effects of the anti-TNF antibody adalimumab in rheumatoid arthritis (RA) by examining synovial tissue and its direct effect on osteoblasts and osteoclasts. - Source: PubMed
Publication date: 2026/07/23
Krishnamurthy AkilanRevu ShankarNeregård PetraHensvold AaseAf Klint ErikMakrygiannakis DimitriosCatrina Anca IParodis Ioannis