Ask about this productRelated genes to: TRAF1 Blocking Peptide
- Gene:
- TRAF1 NIH gene
- Name:
- TNF receptor associated factor 1
- Previous symbol:
- -
- Synonyms:
- EBI6
- Chromosome:
- 9q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-12
- Date modifiied:
- 2016-10-05
Related products to: TRAF1 Blocking Peptide
Related articles to: TRAF1 Blocking Peptide
- Magnetite nanoparticles (FeO NPs), due to their unique physicochemical properties, are considered as promising nanomaterials for multiple biomedical applications. However, the development of novel strategies for surface modification and coating of FeO NPs is needed to fabricate FeO NPs with improved biocompatibility. In the present study, two polymers, namely, poly(ε-caprolactone) (PCL) and poly(ethylene oxide) (PEO), were applied to produce PCL/PEO microfibers containing FeO NPs (PCL/PEO/FeO MFs) using the electrospinning method. Their physicochemical properties, especially magnetically induced hyperthermia effects, were compared to FeO NPs. The biocompatibility and immunocompatibility of PCL/PEO/FeO MFs were then tested using four types of human immune cells, namely, CD14+ monocytes, CD4+ helper, CD8+ cytotoxic T cells, and CD56+ NK cells. Monocytes were the most sensitive to PCL/PEO/FeO MFs as judged by the induction of cell death (apoptosis and necrosis) and micronuclei production, whereas other immune cells were less or not affected by the stimulation with PCL/PEO/FeO MFs. PCL/PEO/FeO MFs also did not lower the viability of normal human fibroblasts. Furthermore, a mild immunogenic response was revealed in PCL/PEO/FeO MF-treated helper T cells based on the analysis of transcriptional activity of 92 genes involved in the NFκB pathway. Observed elevated mRNA levels of , , , , and may have context-dependent immunomodulatory effects in PCL/PEO/FeO MF-stimulated helper T cells that should be taken into account while designing novel drug-delivery systems based on PCL/PEO and FeO NPs. - Source: PubMed
Publication date: 2026/04/15
Radoń AdrianDeręgowska AnnaCiuraszkiewicz AgnieszkaHawełek ŁukaszSpałek HannaWarski TymonHudecki AndrzejŁukowiec DariuszPiotrowski PiotrKrogul-Sobczak AgnieszkaRost-Roszkowska MagdalenaChajec ŁukaszPieszko WeronikaBukała JuliaRzeszutek JuliaWnuk MaciejLewińska Anna - Helicobacter pylori (H. pylori) has been identified as a pathogenic factor in gastric cancer (GC). Building on our previous findings that VacA upregulates TRAF1, which in turn transcriptionally activates OASL, we explored the role of this TRAF1-OASL-PANoptosis axis in GC using clinical samples, cell lines, and mouse models. Functional assays (CCK-8, colony formation, migration, invasion, TUNEL) demonstrated that TRAF1 promotes GC cell proliferation, migration, and invasion via OASL, while suppressing apoptosis. RNA-seq revealed that upregulation of TRAF1 and OASL, combined with H. pylori infection in gastric epithelial cells, enriched pathways associated with PANoptosis. Rescue experiments showed that TRAF1 knockdown increased PANoptosis, and this increase was attenuated by the pan-caspase inhibitor Z-VAD-FMK, whereas subsequent OASL overexpression reversed the suppression of PANoptosis caused by TRAF1 knockdown, whereas LPS further induced PANoptosis. Both in vitro and in vivo models confirmed that H. pylori infection triggers PANoptosis. Co-Immunoprecipitation assays uncovered a protein interaction between OASL and the ZBP1-PANoptosome. Critically, under H. pylori infection conditions, OASL overexpression rescued the PANoptosis suppressed by TRAF1 knockdown in gastric epithelial cells. This study demonstrates that H. pylori infection induces PANoptosis, and defines a pathway wherein TRAF1 promotes PANoptosis by regulating OASL-mediated activation of the ZBP1-PANoptosome. Our findings reveal a novel, context-dependent duality of the TRAF1/OASL axis: it promotes PANoptosis, contributing to mucosal damage during the precancerous inflammatory stage, yet in established GC, this axis appears to suppress PANoptosis, facilitating tumor progression. These insights provide a theoretical foundation for targeting this pathway in treating H. pylori-associated gastritis-cancer progression. - Source: PubMed
Publication date: 2026/04/06
Zhang MinglinYang XueerXie JieCai TingZhao XuelinLiu XiaomingWang Fen - Recovery from coronavirus disease 2019 (COVID-19) probably leads to long-term symptoms, including immune system complications. Recent publications have reported that severe acute respiratory syndrome-associated coronavirus-2 (SARS-CoV-2) infection or, sometimes, vaccination against it may trigger autoimmune responses in vulnerable cohorts. To investigate the differences in the expression of the Protein tyrosine phosphatase non-receptor type 22 (PTPN22), Tumor necrosis factor receptor-associated factor 1 (TRAF-1) and Interleukin-1 beta (IL-1β) genes in patients with rheumatoid arthritis (RA) and healthy controls following SARS-CoV-2 infection or vaccination. Blood samples were collected from 61 patients diagnosed with RA post COVID-19 Rheumatoid arthritis patients after SARS-CoV-2 infection (RAI), and 40 controls (C) who had experienced at least one COVID-19 infection. RNA was extracted and used to prepare cDNA from each sample and was then used to analyse the expression of PTPN22, TRAF-1 and IL-1β using relative gene expression. The study covered all 61 patients; 17 had been vaccinated without prior COVID-19 infection Rheumatoid arthritis patients after SARS-CoV-2 vaccination (RAV), while 44 were diagnosed with RA after recovery from COVID-19 (RAI). A statistically significant decrease in the gene expression of TRAF-1 was observed in both RAI and (RAV) patients compared with the C group (=0.042). A consistently significant increase in gene expression of IL-1β was observed in both RAI and RAV samples compared with controls. However, the reduction in PTPN22 expression was not statistically significant. In this study, TRAF-1 was significantly downregulated, but IL-1β was upregulated in patients with RA post either COVID-19 infection or vaccination, while PTPN22 showed a non-significant reduction. The study findings suggest that triggered immune response post SARS-CoV-2 exposure, through infection or vaccination, may influence molecular pathways involved in RA pathogenesis. - Source: PubMed
Publication date: 2026/04/02
Sanguor Maryam HassanAtwan Hatham WMihan Alsulaitti Saad WaheedRabeeah Iman HusseinAtwan Zeenah W - Equus caballus is a species of considerable economic and cultural significance. However, the regulatory networks involved in equine sexual maturation remain unclear and eventually limit its reproduction and utilization. In this study, testicular tissues from eight Kazakh horses at two developmental stages (2 years, representing pre-maturation, and 3 years, representing post-maturation) were analyzed using whole transcriptome sequencing, data-independent acquisition (DIA) proteomics, and untargeted metabolomics. An integrated regulatory network was constructed encompassing ceRNA, mRNA, protein, and metabolite interactions. Transcriptome analysis revealed that significantly changes circRNAs, LncRNAs, including eca-miR-34-5p, eca-miR-34c, eca-miR-449a, eca-miR-486-3p, and target genes such as TRAF1, TRAF3, ALPK3, SLC29A4 and CPNE3. A total of 277 differentially expressed genes were identified at both the mRNA and protein levels, which are primarily involved in biological processes including PI3K-AKT signaling, focal adhesion, extracellular matrix (ECM) receptor interactions, phospholipase D signaling, and ovarian steroidogenesis. LncRNAs and circRNA were found to modulate COL1A1 expression by competitively binding to miR-7844-x and regulating SPARC through interactions with eca-miR-146-5p and eca-miR-328. Integrated proteomic and metabolomic analyses highlighted TAP1, COL14A1, PRDX3, and SEBENP1 central proteins, along with key metabolites such as guanosine, Austocystin B, methanone, and glycerophosphocholine. These molecules were mainly enriched in pathways related to ovarian steroidogenesis, steroid hormone biosynthesis, and propionate metabolism. In conclusion, this study presents a comprehensive regulatory network involving LncRNA, circRNA, miRNA, mRNA, proteins, and metabolites during equine testicular development. The findings provide novel insights into the molecular basis of equine sexual maturation and offer a valuable foundation for improving reproductive regulation and breeding efficiency in horses. - Source: PubMed
Publication date: 2026/04/02
Yang XixiWen LiuxiangWen MingyueYao XinkuiMeng JunZeng YaqiRen Wanlu - Variants in (which encodes the p65 subunit of NF-κB) can cause a monogenic autoinflammatory disease with clinical manifestations that range from mucocutaneous lesions (Behçet's disease-like) to systemic inflammation. However, the diversity of the phenotype and its penetrance are uncertain. - Source: PubMed
Publication date: 2026/02/18
Hou LingYin LuZhao ChengguangDu Yue