RELB antibody - middle region (P100787_P050)
- Known as:
- RELB (anti-) - middle region (P100787_P050)
- Catalog number:
- p100787_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RELB antibody - middle region (P100787_P050)
Related genes to: RELB antibody - middle region (P100787_P050)
- 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 - middle region (P100787_P050)
Related articles to: RELB antibody - middle region (P100787_P050)
- Interleukin (IL)-1β is a pro-inflammatory cytokine implicated in sterile inflammation and tumor development. Investigating the role of MAPKAP kinase 2 (MK2) in IL-1β processing, we found that mRNA and IL-1β protein levels were elevated in resting -knockout (KO) macrophages and in the serum of double-KO mice. This was linked to activation of the non-canonical NF-κB pathway in the absence of MK2 or its activator, p38α. Rescue by MK2, its kinase-inactive mutant MK2K79R, or p38α suppressed this pathway and reduced expression. We also observed decreased basal protein levels of tumor suppressor p53 in - or -deficient cells. Mechanistically, p53 interacts with caspase-3, promoting cleavage of RelB, thereby inhibiting non-canonical NF-κB signaling and subsequent and expression. These findings explain elevated basal IL-1β levels in -KO macrophages and uncover a new autoregulatory mechanism of expression. Additionally, they reveal a new mechanism that contributes to the long-discussed link between cancer and inflammation, wherein the tumor suppressor p53 inhibits cytokine production in parallel. - Source: PubMed
Publication date: 2026/04/02
Herr Sarah MStalkopf DianaPadaszus SofieHerbst Lukas ADörrie AnnekeNiedenthal RainerRonkina NataliaYakovleva TatianaKotlyarov AlexeyGaestel Matthias - Although pediatric asthma is closely associated with dysregulated inflammatory cytokines, integrated analyses of inflammatory cytokine-related genes and their potential diagnostic biomarkers remain limited. - Source: PubMed
Publication date: 2026/04/07
Gao Mi MiWang XueYin LiWei Xiao YingLi Fang - As a master of host-cell reprogramming, ( ) tachyzoites manipulate diverse signaling networks to establish a niche permissive for long-term infection. While the parasite's subversion of canonical NF-κB signaling (p65/p50) is well established, how infection impacts the non-canonical NF-κB pathway has been largely unexplored. Here, we report that infection induces robust nuclear accumulation of the non-canonical NF-κB subunits RelB and p52 in both human and murine cells. This activation follows a gradual kinetic profile and is conserved across both Type I and Type II parasite genetic backgrounds. We demonstrate that this reprogramming is strictly dependent on the MYR1-dependent export of dense granule effectors. Mechanistically, infection drives the depletion of the negative regulator TRAF3, leading to the stabilization of NF-κB-inducing kinase (NIK), phosphorylation of p100, and its subsequent processing into p52. Utilizing a panel of combinatorial knockout parasites, we reveal that no single effector is responsible for this phenotype. Instead, a suite of eight MYR1-dependent effectors, IST, NSM, HCE1/TEEGR, GRA16, GRA18, GRA24, GRA28, and GRA84, functions through a collaborative, additive network to trigger the non-canonical response. These findings highlight a distributed regulatory strategy used by the parasite to overcome host transcriptional robustness and shape host signaling. - Source: PubMed
Publication date: 2026/03/12
Berg KennaPanas MichaelKurup Samarchith PBoothroyd John CRosenberg Alex - The accumulation of senescent cells contributes to age-related inflammation and heightened susceptibility to viral infection. The mechanisms by which cellular senescence and aging exacerbate virus-associated diseases remain poorly understood. Here we show that innate antiviral immunity is progressively impaired with aging in mice, in parallel with systemic accumulation of senescent cells. Mechanistically, senescent cells suppress innate antiviral response mostly via four senescence-associated secretory phenotype (SASP) factors. GDF15 and IGF1 trigger AKT-MEK-mediated inactivation of GSK3β, leading to suppression of the TBK1-IRF3 axis. IL1α and IL6 induce expression of p52 and RelB to suppress transcription of antiviral genes. Consistently, combined blocking of GDF15, IGF1, IL1α, and IL6 promotes innate antiviral immunity in aged mice. These findings reveal that SASP factors antagonize innate antiviral immunity through distinct pathways and suggest a potential strategy to restore immune competence to defend viral infection in aged individuals by targeting the four SASP factors. - Source: PubMed
Zhang XuZhang QiWang LiLi ShuShu Hong-Bing - Myoblast fusion is essential for skeletal muscle growth and repair, yet the upstream signals regulating this process remain incompletely understood. Here, we show that the cytokine TWEAK promotes myotube formation through activation of alternative NF-κB signaling. Transcriptomic profiling of TWEAK-treated myotubes reveals upregulation of Myomixer (Mymx) and the chemokine CXCL10, both critical for fusion. Mechanistically, the NF-κB member RelB directly binds the Mymx and Cxcl10 gene promoters, enhancing their transcription. Genetic or pharmacological disruption of this pathway impairs myoblast fusion in both C2C12 and primary mouse myoblasts, while Mymx overexpression rescues fusion in TWEAK-deficient myoblasts. In mouse models, TWEAK treatment enhances myotube formation during muscle regeneration, whereas loss of TWEAK reduces fusion efficiency. These findings identify TWEAK-alternative NF-κB signaling as a key regulator of muscle cell fusion through direct transcriptional control of Mymx and Cxcl10 and defines targetable pathways to enhance repair in muscle disease. - Source: PubMed
Publication date: 2026/04/02
Lala-Tabbert NeenaHumphrey AllanRatsun DianaEarl NathalieSt-Jean MartineLaCasse Eric CKorneluk Robert G