TRAF6 antibody - middle region (ARP30226_P050)
- Known as:
- TRAF6 (anti-) - middle region (ARP30226_P050)
- Catalog number:
- arp30226_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TRAF6 antibody - middle region (ARP30226_P050)
Related genes to: TRAF6 antibody - middle region (ARP30226_P050)
- Gene:
- TRAF6 NIH gene
- Name:
- TNF receptor associated factor 6
- Previous symbol:
- -
- Synonyms:
- RNF85
- Chromosome:
- 11p12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-12
- Date modifiied:
- 2015-11-20
Related products to: TRAF6 antibody - middle region (ARP30226_P050)
Related articles to: TRAF6 antibody - middle region (ARP30226_P050)
- 6PPD-quinone (6PPD-Q), a transformation product of the tire antioxidant 6PPD, is an emerging traffic-related contaminant with well-documented ecotoxicity in aquatic species. Its recent detection in airborne particulate matter, road dust, and human urine has raised concerns about possible human health effects. However, its cardiotoxicity in mammalian cells remains poorly understood. Here, we integrated network toxicology, molecular modeling, and in vitro experiments to investigate the effects of 6PPD-Q on the human AC16 cardiomyocyte cell line and the underlying mechanisms. Network toxicology identified 144 putative targets associated with 6PPD-Q-induced cardiotoxicity, with TP53 ranked as the top hub gene, followed by TRAF6, MAPK1, SQSTM1, TNF, and IL6. Enrichment analysis highlighted oxidative stress, inflammation, apoptosis, and autophagy regulation as key biological processes. Molecular docking suggested potential interactions between 6PPD-Q and these hub proteins, while molecular dynamics simulation supported the dynamic stability of the predicted 6PPD-Q-p53 complex. Experimentally, 6PPD-Q induced marked ROS accumulation in AC16 cells, with an IC50 of 13.92 μM after 24 h exposure. It also promoted p53 phosphorylation at Ser15 without increasing total p53 protein or TP53 mRNA expression, indicating stress-associated post-translational activation of p53. This response was accompanied by TRAF6 upregulation, enhanced MAPK1 phosphorylation, and increased IL6 and TNF expression and secretion, supporting the activation of inflammatory stress signaling. Functionally, 6PPD-Q triggered mitochondrial apoptosis, as indicated by mitochondrial membrane potential loss, an increased Bax/Bcl-2 ratio, and activation of cleaved caspase-9 and cleaved caspase-3. In addition, 6PPD-Q disrupted autophagy homeostasis, as evidenced by LC3-II accumulation, p62 depletion, reduced SQSTM1 mRNA expression, increased yellow LC3 puncta, and decreased red-only puncta, suggesting autophagosome accumulation with impaired late-stage autophagic flux. Pharmacological inhibition of p53 by Pifithrin-α (PFTα) attenuated 6PPD-Q-induced inflammatory responses, MAPK1 phosphorylation, mitochondrial apoptosis, and SQSTM1 transcriptional suppression, supporting the functional involvement of p53-related stress signaling. Collectively, these findings show that 6PPD-Q induces cardiomyocyte injury through a p53-associated stress network linking oxidative stress, inflammatory signaling, mitochondrial apoptosis, and autophagy dysregulation, providing mechanistic insight into its potential cardiovascular relevance. - Source: PubMed
Publication date: 2026/09/07
Lu AimeiHuang KailinLi MengfanLu YingdongCha SunaZhang YaniHu XiaomengJi XingXue XinyuWu HuanlinLi HongzhengLi Wei - Systemic lupus erythematosus (SLE) is a chronic autoimmune disease frequently associated with accelerated bone loss and osteoporosis. Emerging evidence implicates the NLRP3 inflammasome as a pivotal mediator of inflammation-driven bone remodeling dysregulation in SLE. This study investigates the therapeutic potential of targeting NLRP3 inhibition for SLE treatment using both a synthetic NLRP3 inhibitor (MCC950) and a natural NLRP3 inhibitor-oridonin, for its potential clinical translation. Using a combination of and approaches, we demonstrate that NLRP3 activation by lipopolysaccharide (LPS) promotes osteoclast differentiation and inhibits osteogenic differentiation through distinct molecular mechanisms. In RAW264.7 macrophages, LPS-induced NLRP3 activation upregulates autophagy-related genes (LC3B, p62) and osteoclastogenesis- related genes (TRAF6, c-Jun, NFATc1), which are effectively suppressed by MCC950 intervention. In mesenchymal stem cells, LPS exposure impairs osteogenic differentiation by reducing Runx2 and OCN gene expression while increasing pyroptosis-related genes (GSDMD, Caspase-11), these effects that are significantly ameliorated by oridonin intervention. In an SLE murine model (MRL/lpr mice), 12 weeks of NLRP3 inhibition with either MCC950 or oridonin both restore bone microstructure, enhance trabecular bone density, improve biomechanical properties, and normalize serum biomarkers of bone turnover. This study provides compelling evidence that targeting NLRP3 signaling represents a promising therapeutic strategy for SLE-associated osteoporosis. The osteogenic effect of oridonin, a naturally occurring compound with established clinical safety, highlights its potential as a promising agent for treating bone loss in SLE patients. These findings underscore the importance of inflammasome targeting in managing SLE-induced bone remodeling disorders. - Source: PubMed
Publication date: 2026/08/22
Deng FeifuLiao YutingGuo WeixiongZhong XiangxinGao XiangAhmad Liu YanzhiWei Jinsong - The integrity of the intestinal mucosal barrier is critical in the pathogenesis of Inflammatory Bowel Disease (IBD). While Astragaloside IV (ASIV) possesses potent anti-inflammatory properties, its specific effects on intestinal epithelial barrier function and the underlying mechanisms involving the Myosin Light Chain Kinase (MLCK) and Myeloid Differentiation Primary Response 88/TNF Receptor-Associated Factor 6 (MyD88/TRAF6) pathways in colitis remain elusive. This study aimed to investigate the protective effects of ASIV on tight junction (TJ) proteins and inflammatory signaling in dextran sulfate sodium (DSS)-induced colitis. - Source: PubMed
Publication date: 2026/08/21
Yang MingyueWang YangJia WenxiuDuan ZhiyingWang JingHuo XiaohuiXu ShunjiangDuan YangyangZhang Xiaolan - TRAF6 is traditionally recognized as an antiviral ubiquitin E3 ligase that positively regulates the production of type I interferon and inflammatory cytokines. However, our study reveals that TRAF6 also plays a crucial role in the lytic replication of Kaposi's sarcoma-associated herpesvirus (KSHV). Mechanistically, during KSHV lytic replication, TRAF6 mediates the K63-linked polyubiquitination and activation of Akt, which is required for the efficient viral replication. Disruption of TRAF6 or Akt expression through CRISPR-mediated knockout, or inhibition of TRAF6 or Akt with small molecule inhibitors, reduces KSHV replication efficiency. Conversely, expression of constitutively active Akt can rescue the impaired replication caused by TRAF6 deficiency. Notably, the TRAF6-Akt axis is also required for the lytic replication of Epstein-Barr virus but not for Human cytomegalovirus. These findings highlight the role of the TRAF6-Akt axis in the life cycle of oncogenic herpesviruses and suggest potential therapeutic targets for related diseases. - Source: PubMed
Publication date: 2026/09/01
Liu ZhenshanGuo QingyuWang WeiliLu HongjiaYu TianyuLi TingtingLiang Qiming - Interferon regulatory factors (IRFs) are DNA-binding transcription factors involved in immune regulation, yet the composition and physiological relevance of IRF repertoires in bivalve molluscs remain incompletely understood. In this study, comparative genomic, phylogenetic, structural and transcriptomic analyses were integrated to examine IRF evolution and immune-associated expression in bivalves. IRF genes were identified from representative bivalve proteomes and analyzed together with IRFs from model animals and previously characterized molluscan sequences. The dataset comprised 29 bivalve species from 12 families. Within this sampled dataset, IRF copy number ranged from two to four per species, with most species retaining three members, indicating a restricted IRF repertoire. Phylogenetic analysis of 113 IRF proteins from 34 species resolved four major subfamilies. Bivalve IRFs were mainly assigned to IRF1/2-like and IRF4/8/9-related lineages, whereas in the present dataset, clear bivalve representatives of vertebrate IRF3/7 and IRF5/6 clades were not detected. Motif and gene-structure analyses indicated conservation of the N-terminal IRF DNA-binding region, while the middle and C-terminal regions were more variable, particularly in IRF4/8-like members. In the noble scallop Mimachlamys nobilis, IRF genes and selected IRF-related genes, including MyD88, TRAF6-like, TBK1/IKKε-like and IKKα/β-like candidates, showed gene-specific expression patterns across tissues, with several genes reaching their highest mean expression in the gill, and showed distinct temporal expression profiles over 72 h of Vibrio parahaemolyticus exposure. Re-analysis of oyster and mussel transcriptomes further showed that IRF genes were expressed together with adaptor and kinase genes under bacterial exposure or in gill-associated immune contexts. These findings suggest that bivalves maintain a restricted but immune-relevant IRF repertoire, and that the potential functional diversification of molluscan IRFs is likely shaped by structural divergence, tissue-biased deployment and differential association with upstream innate immune signaling components rather than by extensive gene-family expansion. - Source: PubMed
Publication date: 2026/08/25
Liao WeiminXie ZekunLiu ShitongSu HailongHu HaixinHe QiqiXu TianyiZhang HongkuanZheng Huaiping