RELB antibody - N-terminal region (ARP37870_T100)
- Known as:
- RELB (anti-) - N-terminal region (ARP37870_T100)
- Catalog number:
- arp37870_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RELB antibody - N-terminal region (ARP37870_T100)
Related genes to: RELB antibody - N-terminal region (ARP37870_T100)
- Gene:
- RELB NIH gene
- Name:
- RELB proto-oncogene, NF-kB subunit
- Previous symbol:
- -
- Synonyms:
- REL-B
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-02
- Date modifiied:
- 2016-04-29
Related products to: RELB antibody - N-terminal region (ARP37870_T100)
Related articles to: RELB antibody - N-terminal region (ARP37870_T100)
- Doxorubicin (DOX) is a widely used chemotherapeutic agent whose clinical utility is restricted by cumulative cardiotoxicity. Vericiguat, a soluble guanylate cyclase stimulator approved for the treatment of heart failure, has shown cardioprotective potential; however, the underlying metabolic and epigenetic mechanisms that contribute to its protective effects against DOX-induced myocardial injury remain unclear. The treatment suppressed the expression of key glycolytic enzymes, including HK2, PKM, LDHA, and LDHB, reduced lactate accumulation, and reversed increased histone lactylation at multiple sites. Integrated Cut&Tag and RNA-seq analyses identified RELB as a histone lactylation-associated gene suppressed by Vericiguat. Functional assays demonstrated that overexpression of RELB diminished the protective effects of Vericiguat, reinstating glycolytic activation, histone lactylation, and inflammatory responses. Conversely, RELB knockdown mimicked the protective effects of Vericiguat and largely eliminated the additional effects of Vericiguat on glycolysis, histone lactylation, inflammation, oxidative stress, cell viability, and apoptosis. In vivo, Vericiguat improved myocardial morphology and alleviated apoptosis and inflammation in DOX-treated mice. These findings demonstrate that Vericiguat mitigates doxorubicin-induced myocardial injury through metabolic-epigenetic regulation involving glycolysis, histone lactylation, and RELB, suggesting a potential therapeutic strategy for anthracycline-induced cardiotoxicity. - Source: PubMed
Publication date: 2026/06/09
Tian GePan JinhuaXie ZifengQu WeiLuo RuZhou Lina - Inborn errors of immunity (IEIs) affecting the NF-κB pathway impair innate and/or adaptive immune responses and may present with or without developmental abnormalities. In this review, we summarize our recent findings from two studies. Monoallelic variants in the RELA gene that result in haploinsufficiency have been linked to tumor necrosis factor-dependent chronic mucosal ulcers and autoimmune cytopenias. However, we have identified a novel form of IEIs caused by dominant-negative RELA mutations, which lead to chronic mucocutaneous ulcerations accompanied by additional autoinflammatory and autoimmune features. Notably, patients exhibit increased expression of Toll-like receptor 7 (TLR7) and MYD88 mRNA in both plasmacytoid dendritic cells and non-plasmacytoid myeloid dendritic cells, resulting in heightened TLR7-mediated production of type I interferons (IFNs). This study provides a mechanistic link between previously distinct groups of IEIs: those involving the NF-κB pathway and those classified as type I interferonopathies. RelB is a critical molecule involved in immune regulation through the non-canonical NF-κB pathway. We describe two families with RelB deficiency caused by novel variants, and we performed detailed functional analyses. As a result, inherited human RelB deficiency disrupts the non-canonical NF-κB pathway, underlying a T- and B cell immunodeficiency, which, together with neutralizing autoantibodies against type I IFNs, confers a predisposition to viral, bacterial, and fungal infections. - Source: PubMed
Moriya Kunihiko - The progression of prostate adenocarcinoma (PCa) toward castration resistance involves complex molecular pathways. This study evaluates the role of NF-κB and EGF receptors (EGFR, HER3) in tumor aggressiveness among Moroccan patients. A retrospective study with immunohistochemical analysis of NF-κB subunits (p65, p50, RelB), EGFR, and HER3 was performed on tissue samples from 88 PCa patients. Results were correlated with castration resistance status and Gleason scores (using Chi-square tests and logistic regression). Strong nuclear localization of NF-κB was detected in castration-resistant cancer cells (p = 0.0005), serving as a predictive marker for progression. Simultaneously, high EGFR expression was identified in hormone-refractory patients (OR = 5.37; p = 0.0010). Nuclear HER3 expression significantly correlated with high Gleason grades (≥ 7) in resistant tumors (p = 0.0064). Nuclear activation of NF-κB and HER3, along with EGFR overexpression, plays a critical role in hormonal escape. These molecules represent promising therapeutic targets and prognostic biomarkers for high-risk PCa management in Morocco. - Source: PubMed
Publication date: 2026/03/26
Sadaoui IlhamSadaoui ImaneJoutei Hanaa Amrani HassaniBenomar HakimaNadifi Sellama - Bushen Bitong Recipe (BSBT) is a traditional Chinese medicine used clinically for osteoarthritis, while bone marrow mesenchymal stromal cell (BMSCs) therapy is increasingly applied for its immunomodulatory and anti-inflammatory properties. However, their combined effects on osteoarthritis have not been investigated. In this study, BSBT containing serum reversed IL-1β induced apoptosis and improved the viability of BMSCs and chondrocytes. Co-treatment with BSBT and BMSCs further enhanced chondrocyte viability and migration, as shown by CCK-8 and Transwell assays. In vivo, X-ray imaging and histological staining (H&E and toluidine blue) demonstrated that the combined therapy preserved joint space, reduced osteophyte formation, and maintained cartilage structure with a more organized arrangement of chondrocytes. At the mechanistic level, TUNEL staining revealed that the combined treatment markedly reduced chondrocyte apoptosis in articular cartilage compared with osteoarthritic controls. These findings were consistent with Western blot analysis, which showed decreased expression of pro-apoptotic proteins Bax and cleaved caspase-3 after co-treatment. Immunofluorescence staining further demonstrated reduced tissue level expression of TLR4, MyD88, and phosphorylated RelB (-RelB), indicating attenuation of TLR4/non-canonical NF-κB signaling. Western blot and ELISA analyses supported these observations, showing suppression of TLR4/p-RelB and a concomitant decrease in pro-inflammatory cytokines and oxidative stress. Overall, these results suggest that BSBT and BMSCs exert synergistic protective effects on cartilage by reducing chondrocyte apoptosis and dampening inflammatory signaling, representing a promising therapeutic strategy for knee osteoarthritis. - Source: PubMed
Publication date: 2026/05/16
Xiang WenyuanXiang ChengIslam AtikulYi LinOuyang ZhengxiaoFang Rui - Chronic kidney disease (CKD) is associated with a substantially elevated risk of mortality. Although GrimAge acceleration (GAA) and metabolic syndrome (MetS) are both implicated in this risk, their combined impact and the underlying biological mechanisms remain poorly understood. - Source: PubMed
Publication date: 2026/05/26
Dang XiangyunJin ZhongxinZhao YafengWang YuLi XianchengLiu XiaoyuanYan PeiXu WeiLiu YuhuiYu XiaoyongZhang Nan