RelB
- Known as:
- RelB
- Catalog number:
- 000125A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- RelB
Related genes to: RelB
- 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
Related articles to: RelB
- Morphological remodeling accompanies the emergence of persister states in some bacteria, yet the regulatory mechanisms underlying these changes remain poorly defined. is an emerging probiotic bacterium that exhibits pronounced phenotypic heterogeneity under antibiotic stress. Here, we show that exposure to chloramphenicol (CAP) activates the type II toxin-antitoxin module RelBE in and is associated with growth arrest and marked cellular elongation in a subpopulation of cells. RelBE consists of the mRNA endonuclease RelE and its cognate antitoxin RelB. Under non-stress conditions, RelBE is maintained at low levels as a non-toxic complex. CAP treatment induces the ClpXP protease, promoting RelB degradation, and transiently increasing free RelE. RelE activity coincides with coordinated transcriptional remodeling of pathways governing cell wall and membrane biogenesis, suppression of core cell division genes, and induction of biofilm-associated programs. These changes are accompanied by compromised cell wall integrity, membrane depolarization, enhanced aggregation, and inhibition of septation, collectively providing a mechanistic basis for the observed elongation phenotype. Rather than establishing a universal role for RelBE in persister formation, our results define how RelE activity reshapes cellular morphological architecture under antibiotic stress. This work links toxin-mediated mRNA cleavage to envelope remodeling, division blockade, and surface-associated adaptations, offering mechanistic insight into stress-induced morphological plasticity in a probiotic bacterium. - Source: PubMed
Publication date: 2026/05/18
Wang Han-YangXiang Wen-LiangCai TingZhu Hao-YuShi PeiXiong Qiao-Ni - Perioperative immunotherapy has significantly improved outcomes for patients with resectable esophageal squamous cell carcinoma (ESCC). Nevertheless, a substantial proportion of patients develop resistance to immunotherapy. This study aimed to identify biomarkers predictive of perioperative immunotherapy efficacy and elucidate the mechanisms underlying treatment resistance in non-responders with resectable ESCC. - Source: PubMed
Gao LijuanKe Shaobo - Asthma exacerbations (AEs), especially those triggered by respiratory syncytial virus (RSV), remain clinically intractable because of limited treatment options and significant immune heterogeneity. In this study, we investigated the central cellular and molecular mechanisms driving RSV-induced AEs using a house dust mite-sensitized mouse model. Through macrophage depletion, transcriptomic profiling, and pathway inhibition, we identified monocyte-derived macrophages (Mo-Mφs) as key orchestrators of both antiviral responses and inflammatory amplification. Mechanistically, Mo-Mφs upregulate and secrete cathepsin C (CTSC), which in turn activates a previously unrecognized PR3/p38/RELB signaling axis. This axis established a positive feedback loop, sustaining macrophage activation and pathogenic inflammation. Pharmacological inhibition of CTSC disrupted this loop, leading to reduced lung inflammation, mucus hypersecretion, and airway hyperresponsiveness. However, this intervention was accompanied by a measurable compromise in antiviral immunity. This study reveals a previously unrecognized CTSC-driven positive feedback loop in Mo-Mφs as a core pathogenic mechanism underlying RSV-induced AE. These findings identify CTSC as a promising mechanism-based therapeutic target, highlighting the need to carefully balance inflammation control against the preservation of antiviral immunity. - Source: PubMed
Publication date: 2026/05/08
Du XiziWu XinyuYuan LinLuo HuaiqingWang LeyuanLiu HuijunYao YeYao SiqiQin QiuyanZhao QianyuLiu DanXiang YangQin XiaoqunYang MingXiong WeiningLiu Chi - Malaria represents a major global health challenge. Excessive activation of inflammatory response is critical for the pathogenesis of severe malaria. The NF-κB signaling pathway regulates inflammatory responses; saturated anacardic acid (SAA) inhibits NF-κB activation. The aim of this study was to evaluate whether SAA modulated inflammatory mediators in BV-2 microglia and THP-1 monocytes, whose overproduction contributes to the development of severe malaria. Survival rate was assessed in cerebral malaria-susceptible CBA mice infected with Plasmodium berghei ANKA and treated or not with SAA. THP-1 monocytes and BV-2 microglia were incubated with or without SAA and with or without co-incubation with P. falciparum or P. berghei ANKA, respectively. After 24 h, terminal molecules of the NF-κB pathway RelA and RelB, TNF-α, IL-6, IL-8, MCP-1, ROS, NO, COX-2 and 5-LOX were assessed by flow cytometry. SAA increased survival in P. berghei-Infected CBA mice. BV-2 microglia exhibited higher RelB expression than THP-1 monocytes. Co-incubation with Plasmodium and SAA decreased RelB but increased RelA expression in BV-2 microglia, whereas RelA expression increased in THP-1 monocytes. Co-incubation with SAA and Plasmodium decreased TNF-α, IL-8, MCP-1, ROS, NO, and COX-2 expression but increased IL-6 production, all of which are associated with inflammatory responses involved in severe malaria. To our knowledge, this study is the first to demonstrate that SAA modulates the key components of severe malaria immunopathogenesis, particularly TNF-α production, ROS and NO generation in BV-2 microglia and THP-1 monocytes. These findings indicate that SAA may represent a promising adjunct therapy to prevent progression to severe malaria. - Source: PubMed
Publication date: 2026/05/06
Gontijo Andreia Cristina Gonçalves CascaesCorazza DaniloAlbuquerque Lucas Fraga FriaçaCiarlini Ana Carolina Laraiade Oliveira Andressa SouzaMonteiro Natália Ciprianode Oliveira Mariangela SouzaCouto Shirley Claudino PereiraRomeiro Luiz Antonio SoaresBorges Tatiana Karla Dos SantosMuniz-Junqueira Maria Imaculada - N-methyladenosine (mA) modifications play a vital role in hepatocellular carcinoma (HCC) progression. However, the function of mA reader proteins in HCC remains poorly understood. Here, we elucidate the role and mechanism of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) in HCC. In here, we analyzed IGF2BP2 expression in HCC using bioinformatics and clinical samples. The functional role of the IGF2BP2-RELB regulatory axis in HCC progression was assessed through cytological assays and a xenograft HCC mouse model. RNA sequencing, Western blotting, Actinomycin-D assays, and RNA immunoprecipitation (RIP) and methylated RNA immunoprecipitation (MeRIP) assays were performed to investigate the regulatory mechanisms of IGF2BP2 on RELB expression. We found high expression of IGF2BP2 in HCC was positively correlated with poor prognosis. Gain- and loss-of-function assays demonstrated that IGF2BP2 was essential for HCC cell proliferation and migration. IGF2BP2 directly bound to RELB mRNA and enhanced its stability via the KH3/4 domain. Upregulated RELB promoted nuclear translocation of the RELB:p52 dimer, leading to activation of the NF-κB signaling pathway. Furthermore, inhibition of IGF2BP2 and RELB suppressed HCC tumor progression both in vitro and in vivo. Our study demonstrates that IGF2BP2 plays a critical role in HCC progression by stabilizing RELB mRNA and activating the NF-κB signaling pathway. The results suggest that IGF2BP2 may be a potential therapeutic strategy for HCC. - Source: PubMed
Publication date: 2026/05/07
Ma HehuaHong YuxinXu ZhiWeng ZuyiYang YuanxunSong WeiLi Juan