Recombinant Human TNFRSF21
- Known as:
- Recombinant Human TNFRSF21
- Catalog number:
- CG09
- Product Quantity:
- 5x10ug
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Recombinant Human TNFRSF21
Related genes to: Recombinant Human TNFRSF21
- Gene:
- TNFRSF21 NIH gene
- Name:
- TNF receptor superfamily member 21
- Previous symbol:
- -
- Synonyms:
- DR6, CD358
- Chromosome:
- 6p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-27
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human TNFRSF21
Related articles to: Recombinant Human TNFRSF21
- Vascular leakage in sepsis is critical factors in improving the prognosis of septic patients, with limited treatment options targeting underlying molecular mechanisms. Necroptosis is a form of cell death centered around the RIPK1/RIPK3/MLKL pathway, combining both programmed and inflammatory characteristics. However, its role and mechanism in sepsis-induced vascular leakage remain unclear. In vivo and in vitro, CLP and LPS were used to simulate sepsis model. It was found that the expression levels of RIPK1/RIPK3/p-MLKL in septic VECs were significantly increased, and necroptosis inhibitors significantly improved septic vascular leakage. Transcriptomic and Western blot results suggested that TNFRSF21 plays a key role in necroptosis. shTNFRSF21 inhibited the formation of necrosome (RIPK3/p-MLKL) in septic VECs, improved vascular leakage in septic rats, and prolonged their survival time. The compound Phen-DC3 of inhibiting TNFRSF21 and the anesthetic remimazolam, both downregulated TNFRSF21, thereby improving septic vascular leakage. Our results suggest that TNFRSF21-regulated necroptosis plays an important role in septic vascular leakage, and targeting TNFRSF21 inhibition may be a potential therapeutic strategy for septic vascular leakage. KEY MESSAGES: Necroptosis plays a crucial role in sepsis-induced vascular leakage. TNFRSF21 promotes necrosome formation by upregulating RIPK3/p-MLKL, leading to endothelial cell death and disruption of the vascular barrier. The TNFRSF21 inhibitor Phen-DC3 was identified as a compound that improves sepsis-induced vascular leakage, providing a potential new therapeutic strategy for sepsis treatment. The anesthetic remimazolam inhibits TNFRSF21, improving sepsis-induced vascular leakage, offering experimental evidence for the repurposing of existing drugs like remimazolam in the treatment of sepsis. - Source: PubMed
Publication date: 2026/04/23
Wang JuntaoZhang BindanWu YujiaLi WeichaoZhang YuxiBao DaiqinPei HaoyuShi CaifengShe HanWang XiaoyanMao QingxiangYu Cong - The progression of periodontitis is accompanied by destruction of keratinized epithelium, while members of the tumor necrosis factor receptor superfamily (TNFRSF) play critical roles in epithelial repair. This study aimed to elucidate the role of TNFRSF in the pathogenesis and progression of periodontitis. Furthermore, we investigated the mechanisms underlying the repair of epithelial keratinization, with the ultimate aim of translating these insights into clinical therapeutic applications. - Source: PubMed
Zhang WenhaoZhang YulongSun ZhongxuanJin SiyuLiu BinXu FeiLu YutongYang YingWu MingyueSun WansuZhang Hengguo - Fragile histidine triad (FHIT) is a well-known tumor suppressor frequently downregulated in gastric cancer (GC), yet its molecular mechanisms remain insufficiently understood. In this study, we reveal that FHIT expression is significantly reduced during carcinogen-induced malignant transformation of gastric epithelial cells, independent of its diadenosine triphosphate hydrolase activity. Ribosome profiling and polysome analysis demonstrate that FHIT regulates the translation of lysine-specific demethylase 6B (KDM6B), a key epigenetic modulator, without altering its transcription. KDM6B promotes expression of proapoptotic genes, including PUMA, NOXA, GADD45, and TP53, by demethylating H3K27me3 at their promoters. In addition, KDM6B negatively regulates cytokine-related genes, such as TNFRSF12A, TNFSF9, and TNFRSF21. Functional assays, including colony formation, micronucleus assays, and xenograft tumor growth studies, confirm that FHIT's tumor-suppressive effects are independent of its enzymatic activity but rely on translational regulation. Our findings reveal a novel FHIT-KDM6B axis that integrates translational and epigenetic regulation to inhibit GC progression. Targeting this pathway may offer promising therapeutic strategies for early stage GC intervention. - Source: PubMed
Publication date: 2026/03/26
Hu HaoruiWang YumingQi HongyanLiu GuilingWang RunanShen Jing - Axon degeneration (AxD), accompanied by glial remodeling, is a pathological hallmark of many neurodegenerative diseases, leading to the disruption of neuronal connectivity. Understanding the mechanisms in neurons and glia that regulate AxD is essential for developing therapeutic strategies to prevent or mitigate axon loss. Wallerian degeneration (WD) is a well-established model to study the mechanisms of nerve injury-induced AxD, glial responses, and axon-glia interactions. We recently showed that Schwann cells (SCs), the axon-associated glia of the peripheral nervous system, exert protective effects on axons through their rapid metabolic injury response. Enhancing this SC response promotes axon protection during WD. A prior study reported that eliminating the orphan tumor necrosis factor receptor DR6 (death receptor 6, encoded by ) strongly delays AxD and alters SC injury responses during WD, suggesting a possible intersection with our findings. Here, we rigorously revisit the role of DR6 in WD using two independent DR6 knockout mouse lines including the same model used in the previous study. Surprisingly, in contrast to the earlier report, we observed no impact of DR6 deletion on AxD kinetics or SC injury responses across a range of WD assays. Moreover, injured axons in primary neuronal cultures lacking DR6 degenerated at a similar rate as wild-type axons. We conclude that DR6 is dispensable for the regulation of AxD and glial nerve injury responses during WD. Our data argue that any therapeutic benefit from DR6 suppression in neurodegeneration models occurs through mechanisms independent of WD. - Source: PubMed
Publication date: 2026/03/27
Beirowski BogdanHuang HaoranBabetto Elisabetta - Pancreatic cancer represents a significant global health burden. Although dysregulated lipid metabolism and its associated inflammation drive tumorigenesis, their molecular interplay remains incompletely understood. This bioinformatics study investigates lipid metabolism-related genes (LMRGs) for prognostic prediction and treatment guidance in pancreatic cancer. - Source: PubMed
Publication date: 2025/12/26
Xue RunxinTao ZhiweiBai RuiShao YanLiu NaWang Chuying