DcR3 Antibody
- Known as:
- DcR3 Antibody
- Catalog number:
- 2140
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- DcR3 Antibody
Related genes to: DcR3 Antibody
- Gene:
- TNFRSF6B NIH gene
- Name:
- TNF receptor superfamily member 6b
- Previous symbol:
- -
- Synonyms:
- DcR3, DCR3, TR6, M68
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-07
- Date modifiied:
- 2016-11-10
Related products to: DcR3 Antibody
Related articles to: DcR3 Antibody
- Smoking dependence (SD) and Crohn's disease (CD) are epidemiologically associated, but whether this relationship reflects shared genetic susceptibility remains unclear. - Source: PubMed
Publication date: 2026/09/11
Ji AochengXu WenbinXiong HaoZhong HuanZeng Chunyan - Premature ovarian insufficiency (POI) is a leading cause of female infertility. Its mechanisms are poorly understood, and effective therapies are lacking. In this study, we aimed to identify novel druggable targets and repurposable drugs for POI through an integrated multiomics and computational pharmacology approach. We integrated large-scale proteomic data from two independent cohorts (deCODE, N = 35,559; UK Biobank, N = 54,219) using Mendelian randomization, Bayesian colocalization, and single-cell RNA sequencing. Seven high-confidence targets were identified: EPHA4, FSTL3, NUCB2, OXT, SERPINA12, TNFRSF6B, and FABP1. Among these genes, EPHA4, FSTL3, and NUCB2 were significantly dysregulated in cisplatin-induced mouse and human granulosa cell models (P < 0.05 to P < 0.001) and exhibited high diagnostic accuracy (AUC = 0.92-0.96), supporting their potential as both biomarkers and therapeutic targets. Molecular docking revealed strong binding affinities, notably for cycloheximide binding to EPHA4 (-7.8 kcal/mol), with molecular dynamics confirming stable interactions (root mean square deviation, RMSD < 2.0 Å), providing a structural basis for drug repurposing or lead optimization. The functional enrichment results suggested that fibrosis, inflammation, and metabolic dysregulation are involved in POI pathogenesis. Collectively, our findings establish a multiomics-to-therapy pipeline that not only prioritizes causal targets for POI but also provides translational opportunities, from biomarker-guided diagnosis to computationally driven drug repositioning, paving the way for mechanism-based interventions in ovarian aging. - Source: PubMed
Publication date: 2026/08/28
Liu ChaoWang RunzhiLiu XinnongLi YuanRen LiliZhao ZhiyuFan ZhongkaiXiao Jianying - Tumor necrosis factor-like cytokine 1A (TL1A, TNFSF15) is a profibrotic and proinflammatory cytokine. Experimental evidence implicates TL1A-mediated interactions in interstitial lung disease (ILD); such interactions are disrupted by decoy receptor 3 (DcR3) binding to TL1A. We examined the potential clinical value of circulating TL1A and DcR3 levels in systemic sclerosis (SSc). - Source: PubMed
Publication date: 2026/08/20
Poulia VassilikiVlachogiannis Nikolaos IAvdi Aikaterini-ParaskeviBournia Vasiliki-KalliopiBamias GeorgeTektonidou Maria GSfikakis Petros PPanopoulos Stylianos - Hyperuricemia, characterized by elevated serum uric acid (SUA) levels, is increasingly recognized as a pathological contributor to renal injury through oxidative stress, inflammation, and apoptosis. Hirudin, a thrombin inhibitor derived from leech saliva, has recently been noted for its anti-inflammatory properties, yet its role in hyperuricemia remains unclear. This study aimed to investigate the protective effects and underlying mechanisms of hirudin in a uric acid (UA)-induced renal tubular epithelial injury model. Using HK-2 cells, we found that hirudin enhanced cell viability and reduced apoptosis in UA-treated conditions. Mechanistically, these protective effects were mediated through downregulation of TNFRSF6B, a decoy receptor involved in inflammatory and apoptotic signaling. TNFRSF6B knockdown potentiated hirudin's cytoprotective effects, whereas its overexpression reversed them. Hirudin treatment attenuated UA-induced expression of urate transporters (URAT1, GLUT9, and OAT4) and pro-inflammatory cytokine IL-1β, both at the transcriptional and protein levels. Moreover, hirudin suppressed activation of the NF-κB signaling pathway, a critical mediator of inflammation and apoptosis in hyperuricemia, with transcriptomic and immunoblotting data confirming downregulation of NF-κB-associated targets. Co-treatment with JSH-23, an NF-κB inhibitor, further reinforced these findings and highlighted a TNFRSF6B/NF-κB axis as a key regulatory mechanism. Collectively, these findings reveal a novel protective role for hirudin in UA-induced renal injury, mediated via modulation of TNFRSF6B and suppression of NF-κB signaling. This study provides new insight into the potential therapeutic application of hirudin in hyperuricemia-associated kidney damage. - Source: PubMed
Zhao YingxueQin YongjieHe LanzhiLuo HaikunMo YingZhou WeihaiHe HuameiZhou GanpingLiu Xihua - Osteosarcoma (OSA) is an aggressive primary bone tumor of humans and dogs, with metastatic progression remaining the major determinant of poor outcome. Although serum alkaline phosphatase (ALP) has been investigated as a prognostic marker in OSA, its clinical value remains inconsistent across studies. We examined whether ALP-associated transcriptional programs in canine OSA could capture conserved tumor biology relevant to metastatic behavior in human OSA. Differential expression analysis of a canine OSA RNA-seq cohort, followed by repeated LASSO and Boruta feature selection, identified an 11-gene ALP-associated signature. This signature was mapped to human orthologs and evaluated in two independent human OSA transcriptomic cohorts for metastatic-status classification. Candidate genes were further assessed through structured literature review and dog-human orthology analysis. Across human validation datasets, the canine-derived signature showed moderate but reproducible discrimination of metastatic status, with AUC values of approximately 0.70-0.78 depending on cohort and classifier. Several candidate genes, including KEAP1, CCN3, NACC1, and TNFRSF6B, were linked to metastatic processes such as oxidative-stress response, extracellular matrix remodeling, stemness, immune evasion, and survival under stress. Additional survival analysis in the canine GSE238110 cohort showed that ALP status alone was not a statistically significant prognostic marker, although elevated ALP showed a weak trend toward poorer overall survival. These findings suggest that the signature represents an ALP-associated molecular phenotype rather than a direct serum-ALP prognostic surrogate. This study supports comparative oncology as a discovery framework for prioritizing conserved metastasis-related biomarkers requiring further validation. - Source: PubMed
Publication date: 2026/07/27
Mahawan TanakamolPangprasit NoppasonDewi Putri Krishna KumaraThongratsakul Sukanya