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
- Oral inflammatory diseases affect nearly half of all humans, yet mechanisms underlying rapidly-destructive inflammation remain poorly understood. We compared peri-implantitis with moderate- and high-grade periodontitis using integrated microbial and single-cell sequencing (>967,169-cells; single-cell RNA-seq, spatial proteotranscriptomics). Laser capture microdissection with compartmental microbiome analysis revealed reduced bacterial load and diversity in peri-implantitis. Expansion of the Human Periodontal Atlas with peri-implantitis single-cell RNA-seq data (36-samples; 121,395 cells) identified CD34 vascular endothelial cell (VEC) rarefaction and oxidative stress, hypoxia, and NAD⁺ metabolism-associated transcriptional programs enriched in a TNFRSF6B⁺/ICAM1⁺ post-capillary venule (PC-VEC) subpopulation. NAD⁺-consuming ectoenzyme CD38 was selectively enriched and orthogonally confirmed by spatial transcriptomics (6-samples; 283,377-cells) and proteomics (23-samples; 562,397-cells). Spatial neighborhood analyses demonstrated CD38⁺-high PC-VEC expansion, closer proximity, and higher IL16-CD4 T cell signaling in peri-implantitis. Matched high-grade periodontitis biopsies confirmed spatially restricted CD38⁺-VECs despite similar microbial burden, identifying endothelial vasculopathy underlying rapidly advancing oral inflammation and a potential therapeutic axis. - Source: PubMed
Publication date: 2026/05/08
Easter Quinn THuynh Khoa L AStolf Camila SchmidtXie JialiuMatuck Bruno FHasuike AkiraAlvarado-Martinez ZabdielKim William SChen ZhaoxuRibeiro Apoena AguiarPareek NiveditaAzcarate-Peril Andrea MWu DiCasarin RenatoKo Kang ILiu JinzeByrd Kevin M - Type 2 diabetes (T2D) is a challenge for the healthcare system. It is a metabolic disease with increased blood sugar with severe complications when it becomes uncontrolled. These complications include diabetic nephropathy (DN), neuropathy, retinopathy neuropathy, and cardiovascular diseases (CVDs). T2D is induced by genetic, environmental, and lifestyle risk factors. Therefore, it is vital to distinguish between genetic risk loci for T2D and those that specifically predispose patients to DN, which may eventually facilitate personalized risk assessment and informed genetic counseling once these markers are clinically validated. The aim of this pilot study was to examine the candidate genes associated with DN using whole-exome sequencing (WES). - Source: PubMed
Publication date: 2026/03/26
Mir RashidElfaki ImadeldinAlmassabi Rehab FAlmowallad SanaaElnageeb Mohamed EMirghani Hyder OsmanAlbalawi WedAlbalawi Aziz DhaherAltemani Faisal HBarnawi JameelTayeb Faris JMoawadh MamdohBedaiwi Ruqaiah IAlanazi Mohammad A - Sepsis is a life-threatening syndrome characterized by dysregulated host-immune responses, progressing through hyperinflammatory and immunosuppressive stages. Decoy receptor 3 (DcR3), a soluble member of the TNF receptor superfamily, serves as an immunomodulator in sepsis. Beyond neutralizing FasL, LIGHT, and TL1A to block apoptosis and inflammatory signaling, DcR3 regulates macrophage polarization, dendritic cell maturation, and immune cell survival through its heparan sulfate proteoglycan-binding domain. Evidence from cellular, molecular, and animal studies highlights its dual role in restoring immune balance by modulating both hyperinflammatory and immunosuppressive phases of sepsis. In this review, we summarize current evidence on DcR3 in sepsis and discuss translational challenges and future directions. Current rodent models lacking the TNFRSF6B gene are limited; however, transgenic mice expressing human DcR3 exhibit both protective and detrimental context-dependent effects. Translational challenges include the pharmacokinetics and immunogenicity of recombinant DcR3, although strategies such as PEGylation, nanoparticle encapsulation, and hydrogel delivery may improve its efficacy. Combining DcR3 with PD-1/PD-L1 inhibitors or immunometabolic agents like metformin and dimethyl itaconate presents promising therapeutic potential. Future research will focus on CRISPR/Cas9 knock-in mouse models, multi-omics mapping of DcR3 signaling, and biomarker-guided dosing. Although no DcR3-targeted clinical trials in sepsis have been conducted, DcR3 remains a precision-targeted immunotherapy with mechanistic and translational pathways; this review delineates key knowledge gaps that must be addressed to enable future clinical application. - Source: PubMed
Publication date: 2026/01/26
Abbas BilalLin XinruiXu ChenChen QiSu Jingqian - Despite immunotherapy±chemotherapy has transformed the therapeutic landscape for patients with non-small cell lung cancer (NSCLC), critical questions remain regarding how detailed smoking history affects the evolving treatment options and the underlying molecular mechanisms driving these effects. - Source: PubMed
Publication date: 2025/12/21
Wang XinanRicciuti BiagioElkrief ArielleAlessi Joao VDi Federico AlessandroPecci FedericaNishino MizukiGulhan DogaAnanda GuruprasadRodig Scott JSholl LynetteJohnson BruceLin XihongSchoenfeld AdamAwad Mark MChristiani David - Preeclampsia, a pregnancy-related disorder, has high morbidity and mortality rates. Decoy receptor 3 (DcR3) plays a critical role in immune modulation during pregnancy. This study investigated the functional role of DcR3 in trophoblast cell phenotypes. - Source: PubMed
Publication date: 2025/11/26
Zhao PoLi DanLiu Xiuwei