Rabbit Anti-Human DcR3, C-terminus
- Known as:
- Rabbit Antibody toHuman DcR3, C-terminus
- Catalog number:
- 129-10228
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human DcR3 C-terminus
Related genes to: Rabbit Anti-Human DcR3, C-terminus
- 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: Rabbit Anti-Human DcR3, C-terminus
Related articles to: Rabbit Anti-Human DcR3, C-terminus
- Super-enhancers are clusters of cis-regulatory elements that sustain the expression of cell-identity genes. Their aberrant activation or dysfunction constitutes a hallmark of malignant cellular transformation, which frequently rewires oncogenic transcriptional programs to support uncontrolled cell proliferation and metastatic potential. However, the functions and epigenetic regulation mechanisms of colorectal cancer specific super-enhancers remain poorly understood, and few studies have focused on dissecting how tumor enriched super-enhancers mediate downstream oncogenic signaling in CRC. By integrating multi-omics sequencing data, we identified a highly active super-enhancer in colorectal cancer, termed DCBLD2-SE. Through luciferase reporter assays, the SE3-2 subregion was identified as the minimal functional core of this super-enhancer. Mechanistic studies confirmed that transcription factors of the activator protein-1 family (FOSL2 and JUND) can bind directly to the SE3-2 cis-regulatory element, synergistically regulating local chromatin remodeling and strongly driving the upregulation of the target gene DCBLD2. Following knockout of the DCBLD2-SE core region, the malignant proliferative capacity of colorectal cancer cells decreased significantly, and the growth of xenograft tumors in vivo was markedly inhibited. Functionally, DCBLD2-SE facilitates tumor progression through a DCBLD2-dependent CD146/AKT/TNFRSF6B signaling axis. Clinically, high expression of DCBLD2 correlates with malignant metastasis and poor overall survival in patients with colorectal cancer. In summary, this study uncovers a previously undescribed DCBLD2-centered regulatory cascade that promotes colorectal cancer initiation and progression. DCBLD2-SE and its binding transcription factor activator protein-1 represent promising prognostic biomarkers and actionable therapeutic targets for colorectal cancer. - Source: PubMed
Publication date: 2026/09/23
Wu TongShao LanHu XinHe HongjuanChen LuFeng MeiqiQi ChengjinWang ZiwenYu HaoranJi BoshuCao YijiaZhang YanWu Qiong - Elevated expression of tumor necrosis factor α-induced protein 8 (TIPE) is observed in colorectal cancer (CRC) and is known to regulate decoy receptor 3 (DcR3) expression while promoting M2 polarization of macrophages. However, the precise role of DcR3 in macrophage M2 polarization remains to be elucidated. - Source: PubMed
Publication date: 2026/09/04
Zhang ShiyingShen ChunlinLin ZeyangZhu QiangFeng YihanSun LiweiZhang ChengjiaZhang HaoleWang LuminChen ShuyuHuang JiyiYe YuhanQiu XingfengZhuang Guohong - 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