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)
- The nuclear receptor NOR-1 is a key transcription factor in vascular smooth muscle cells (VSMCs) implicated in the pathogenesis abdominal aortic aneurysm (AAA), a life-threatening disease lacking pharmacological options. Here, we aimed at identifying potential therapeutic targets regulated by NOR-1 in the onset and progression of AAA. RNA-seq analysis in dilated arteries from AngII-infused transgenic mice overexpressing NOR-1 in VSMCs (TgNOR-1) revealed an early transcriptomic signature enriched in immune-inflammatory and tissue remodeling pathways. Biologically informed analysis identified a set of genes (Spp1, Il6, Tnfsf11, Grem1, Fcgr4, Adam8 and Mmp9), linking immune-inflammatory and vascular remodeling pathways, upregulated in TgNOR-1 dilated aortas. Re-analysis of RNA-seq datasets from human AAA aortas revealed the activation of inflammation- and extracellular matrix (ECM)-related pathways, with SPP1 and IL6 as the most upregulated genes in both clusters. In human AAA, NOR-1 expression correlated with that of SPP1 and IL6, while luciferase reporter assays and site-directed mutagenesis indicated that NOR-1 increases SPP1 transcriptional activity. Consistently, gain- and loss-of-function studies showed that NOR-1 regulates SPP1 expression. Integrative co-expression and protein-protein interaction analysis in human AAA identified SPP1 as a critical element at the cross-road between ECM remodelling and vascular inflammation. Inhibition of osteopontin (OPN, encoded by Spp1) with HY-146064 attenuated AngII-induced AAA in TgNOR-1 mice, limiting vascular remodelling, oxidative stress, and inflammation. Overall, we identify NOR-1 as an early driver of transcriptional reprogramming in AAA, establishing the NOR-1/SPP1/OPN axis as a key mediator of the cross-talk between inflammation and vascular remodelling, and a potential therapeutic target for disease intervention. - Source: PubMed
Publication date: 2026/09/25
Vázquez-Sufuentes PaulaAlonso JudithAlmendra-Pegueros RafaelBallester-Servera CarmeGarcía-Aranda JuliánMartín-Fernández LauraCorrales IreneNus MeritxellJiménez-Altayó FrancescVidal FranciscoRodríguez CristinaMartínez-González José - Atopic dermatitis (AD) is a chronic inflammatory disease driven by Type 2 (Th2) inflammation. Dupilumab (anti-IL-4Rα) and tralokinumab (anti-IL-13) are effective biologic therapies, but a direct comparison of their longitudinal effects on the systemic proteome is lacking. This exploratory study aimed to identify and to differentially analyze the proteomic signatures in AD patients treated with dupilumab versus tralokinumab. - Source: PubMed
Francuzik WojciechPažur KristijanWorm Margitta - Rheumatoid arthritis (RA) is associated with accelerated bone loss, partly mediated by dysregulation of the receptor activator of nuclear factor-κB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) pathway, which regulates osteoclast activity. Carboxy-terminal cross-linked telopeptide of type I collagen (CTX-1) is a biochemical marker of bone resorption and may reflect increased skeletal turnover in RA. Although previous studies have evaluated RANKL, OPG, and the RANKL/OPG ratio in relation to bone mineral density, osteoporosis, and fracture risk, the correlations of circulating RANK, RANKL, and OPG with CTX-1 remain insufficiently characterized in patients with RA. The aim of this study was to evaluate the correlations of serum RANK, RANKL, and OPG levels with serum CTX-1 levels in patients with RA. An analytical cross-sectional study was conducted at a provincial referral hospital in Padang, Indonesia, from July to December 2024, during which patients with RA were recruited through consecutive sampling. Serum RANK, RANKL, OPG, and CTX-1 concentrations were measured using enzyme-linked immunosorbent assays. Correlations were assessed using Pearson's correlation analysis. The mean age of the patients was 40.30±5.08 years. The mean serum concentrations of RANK, RANKL, OPG, and CTX-1 were 5.20±2.83, 6.55±3.14, 0.17±0.09, and 2.10±1.10 ng/mL, respectively. Serum RANK and RANKL levels showed very strong positive correlations with CTX-1 levels (=0.928 and =0.929, respectively; both <0.001). Serum OPG levels also showed a strong positive correlation with CTX-1 levels (=0.786; <0.001). These findings suggest that circulating components of the RANK/RANKL/OPG pathway are associated with biochemical bone resorption in patients with RA. However, a larger longitudinal study incorporating disease activity, treatment exposure and bone mineral density is required to determine their clinical relevance. - Source: PubMed
Publication date: 2026/07/27
Najirman NajirmanKurniawan EkaHerdian Herdian - Osteoporosis remains a major global health challenge, and current single-pathway therapies often fail to achieve coordinated bone remodeling. Dickkopf-1 (DKK-1) is a potent inhibitor of the Wnt/β-catenin signaling pathway and plays a critical role in osteoporotic bone loss. Neutralization of DKK-1 represents a promising therapeutic strategy to promote bone formation while simultaneously inhibiting bone resorption. - Source: PubMed
Publication date: 2026/08/27
Hou ShengGao TianyuWu YimeiWang HaoZhang DapengGuo QingchengXu JinGuo HuaizuQian Weizhu - Excessive osteoclast activity drives bone-resorptive disorders, and oxidative stress is a key regulator of osteoclast differentiation. Hydrogen sulfide (H?S), an endogenous antioxidant, may modulate this process, but its mechanisms remain unclear. In this study, RANKL (50 ng/mL) was used to induce osteoclastogenesis in RAW264.7 cells, with or without the H?S donor sodium hydrosulfide (NaHS; 50-200 ?M). Osteoclast formation was evaluated by TRAP staining and NFATc1/Cathepsin K expression, while oxidative stress, lipid peroxidation, mitochondrial function, and ferroptosis-related parameters were assessed. Mechanistic studies revealed that NaHS promoted Nrf2 nuclear translocation and upregulated GPX4, HO-1, and NQO1, whereas inhibition of Nrf2 or GPX4 partially reversed these effects. NaHS significantly suppressed osteoclast differentiation, alleviated oxidative stress, and restored mitochondrial function. These findings demonstrate that H?S inhibits RANKL-induced osteoclastogenesis via the Nrf2/GPX4 pathway and suggest this redox axis as a potential therapeutic target for bone-resorptive diseases. - Source: PubMed
Huang ZelinLai MingWei QinglanCao QiChen KangZhang Jie