RelB (Phospho_Ser552) Antibody
- Known as:
- RelB (Phospho_Ser552) Antibody
- Catalog number:
- E011255-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- RelB (Phospho_Ser552) Antibody
Related genes to: RelB (Phospho_Ser552) Antibody
- 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 (Phospho_Ser552) Antibody
Related articles to: RelB (Phospho_Ser552) Antibody
- We extracted turmeric volatile oil (TVO) from turmeric using supercritical CO₂ extraction for potential allergic rhinitis (AR) therapy. The volatile components of TVO were analyzed using gas chromatography mass spectrometry and gas chromatography-ion migration spectrometry. The pharmacological effects of TVO on ovalbumin (OVA)-induced AR in mice were evaluated through pathological markers, microbiomics, metabolomics, and proteomics. An inflammatory model using human mast cells (HMCs) was established to assess whether TVO could mitigate inflammation. TVO effectively alleviated AR symptoms in OVA-sensitized mice and reduced inflammation in lipopolysaccharide- and interferon-γ-treated HMCs. TVO suppressed the inflammatory cytokine production, restored the nasal microbiota composition, and regulated serum metabolic profiles. Proteomic analysis using four-dimensional data-independent acquisition indicated that the mitogen-activated protein kinase (MAPK) and transcription factor nuclear factor-κB (NF-κB) signaling pathways are involved in TVO's anti-inflammatory mechanism. Accordingly, TVO inhibited the activation of MAPK and NF-κB pathways in the OVA mouse model and the inflammatory HMCs model. Jun N-terminal kinase and Relb were identified as key mediators in the therapeutic action of TVO, with Relb knockdown enhancing its anti-inflammatory effect, suggesting that TVO has potential as a therapeutic agent for alleviating AR. - Source: PubMed
Publication date: 2026/06/18
Shang LiyingBian ShuaiWang XinXu YananWang MingyueZhao DaqingZhang WeiBai Xueyuan - Identification and characterization of novel mechanisms driving melanoma metastases and ways to target them are paramount for the development of effective treatment modalities. Here, we employed in vivo CRISPR knockout screening targeting the genes associated with poor prognosis to identify Polr1a as a potent driver of melanoma metastasis. High Polr1a levels correlate with increased metastasis and reduced survival in patients. Polr1a inhibition suppressed migration, invasion, and the ability of melanoma cells to colonize lungs. Ribo-seq analysis revealed that Polr1a is involved in regulating the non-canonical NF-κB pathway. Indeed, targeting Polr1a decreased levels of RelB and p52 and suppressed non-canonical NF-κB transcriptional activity; this suppression was responsible for the effects of Polr1a on melanoma cell migration. Accordingly, pharmacological inhibition of Polr1/Polr1a suppressed cell migration, tumor growth, and metastases. We discuss the potential utilization of Polr1 inhibitors for neoadjuvant treatment of melanoma. - Source: PubMed
Publication date: 2026/06/17
Fajardo Anna FGowda Chethana PJohnson EmilyPetroni RicardoTomar Vivek SLiu ZhenqiuAndres Blanco MJanssen JacobElcheva Irina ALanza MatthewFuchs Serge YSpiegelman Vladimir S - 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