TRAF1 Monoclonal Antibody [3D4]
- Known as:
- TRAF1 Monoclonal Antibody [3D4]
- Catalog number:
- A-0438-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- TRAF1 Monoclonal Antibody [3D4]
Related genes to: TRAF1 Monoclonal Antibody [3D4]
- Gene:
- SORBS3 NIH gene
- Name:
- sorbin and SH3 domain containing 3
- Previous symbol:
- -
- Synonyms:
- SCAM-1, SH3D4, vinexin
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-28
- Date modifiied:
- 2014-11-19
- 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 Monoclonal Antibody [3D4]
Related articles to: TRAF1 Monoclonal Antibody [3D4]
- Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the intestine caused by multiple factors, with a global incidence that is increasing year by year, severely affecting patients' quality of life. Capsaicin (CAP), the main active component in chili peppers, has anti-inflammatory and antioxidant effects. As a key part of the immune system, macrophages play a critical role in maintaining intestinal homeostasis. Growing evidence suggests that M1 macrophage polarization is closely associated with the onset and progression of IBD. This study used a dextran sulfate sodium (DSS)-induced IBD model, lipopolysaccharide (LPS)-induced macrophage M1 polarization and bone marrow-derived macrophages (BMDMs), and found that CAP can significantly alleviate macrophage M1 polarization by reducing the expression of CD86 and iNOS, inhibiting the release of inflammatory factors tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), and improving intestinal pathological damage. RNA sequencing (RNA-seq) analysis suggested that CAP may act through the TNF receptor-associated factor 1 (TRAF1) /nuclear factor kappa B (NF-κB) pathway, further, silencing TRAF1 with siRNA and AAV confirmed that this pathway plays a key role in CAP regulation of macrophage polarization and alleviation of IBD. This study reveals the molecular pathway by which CAP alleviates IBD through regulating M1 macrophage polarization, providing an important theoretical basis for a deeper understanding of the pathogenesis of IBD and the development of new therapeutic strategies. - Source: PubMed
Publication date: 2026/06/03
Chen LiZhang QiLiu DanLi JieWang NingWu Xin-YiWu Xue-Dong - Ultraviolet (UV) radiation is a major environmental driver of skin photoaging and induces keratinocyte senescence accompanied by the release of senescence-associated secretory phenotype (SASP) factors that promote dermal degeneration. However, whether and how skin commensal bacteria modulate UV-induced senescence remains incompletely understood. Here, we investigated the potential role of , a dominant epidermal commensal, in regulating UV-induced skin photoaging. In a murine photoaging model, intradermal or topical administration of a ≤10 kDa fraction derived from culture supernatant attenuated epidermal hyperplasia, collagen degradation, and the expression of senescence-associated markers following long-term UV exposure. In keratinocytes, UVB irradiation induced reactive oxygen species accumulation, DNA damage, and robust production of SASP factors that promoted paracrine senescence in dermal fibroblasts. Treatment with or its candidate bioactive lipopeptide component LP78 markedly reduced these responses. Genetic deletion or silencing of Toll-like receptor 3 () diminished UV-induced SASP factor production and fibroblast senescence, supporting a role of TLR3 in photoaging-associated inflammatory signaling. Mechanistically, and LP78 activated TLR2 signaling to induce TNF receptor-associated factor 1 (TRAF1), a negative regulator of TLR3, thereby suppressing TLR3-mediated SASP production. Collectively, these findings identify a potential microbiota-innate immune regulatory axis in which -derived factors restrain keratinocyte inflammatory senescence and attenuate UV-induced skin damage. This work highlights a potential role of commensal bacteria in limiting photoaging-associated inflammation. - Source: PubMed
Publication date: 2026/05/12
Wang XinxinWang MengkeYang JingyaLiu WenboJia HaidongChen YuanyuanLai Yuping - To investigate the mechanism of DZ2002, a reversible type III S-adenosyl-l-homocysteine hydrolase (SAHH) inhibitor, in alleviating corneal graft rejection in rats through the downregulation of TRAF1 and modulation of Th17 differentiation, so as to provide a new therapeutic strategy for corneal graft rejection. Rat models of corneal graft rejection were constructed and treated with DZ2002 eye drops. Metabolomics and transcriptomics sequencing analyses were used to identify the key metabolite, homocysteine, and its associated gene, TRAF1. Histological assessments were conducted to evaluate the effect of DZ2002 on corneal graft rejection. Additionally, the underlying mechanism of action was explored through Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Homocysteine emerged as a key metabolite involved in corneal graft rejection, and DZ2002 could significantly decrease the rejection index and reduce the opacity and edema of corneal grafts. The effect of DZ2002 in alleviating rejection was attributed to the downregulation of TRAF1 expression, inhibition of the PI3K/AKT pathway, decreased expression of chemokine CCL5 in the aqueous humor, and suppression of the differentiation of T cells into Th17 cells. DZ2002 was effective in reducing corneal graft rejection in rats by downregulating TRAF1 and modulating Th17 differentiation. - Source: PubMed
Publication date: 2026/01/01
Cao QianLi YongZhang YongqianTan ShuangLong JunjunTian ErmiaoDong JieLi Lan - 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