RelB Antibody (Ab_573), pAb, Rabbit
- Known as:
- RelB Antibody (Ab_573), pAb, Rabbit
- Catalog number:
- A00547
- Product Quantity:
- 200ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- RelB Antibody (Ab_573) pAb Rabbit
Related genes to: RelB Antibody (Ab_573), pAb, Rabbit
- 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 (Ab_573), pAb, Rabbit
Related articles to: RelB Antibody (Ab_573), pAb, Rabbit
- 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 - Influenza A virus (IAV) is an important zoonotic pathogen responsible for substantial respiratory morbidity and mortality. Elucidating the mechanisms by which IAV evades host innate immunity is critical for developing novel antiviral strategies. Although the IAV non-structural protein 2 (NS2) is well-characterized for the export of viral ribonucleoproteins (vRNPs) from the host cell nucleus, the function of NS2 in evading host innate immunity, especially the NFKB/NF-κB (nuclear factor kappa B) signaling pathway, remains poorly understood. The present study uncovered that NS2 is a novel viral inhibitor of the NFKB pathway. Mechanistically, NS2 interacted with and mediated the degradation of the NFKB essential modulator (IKBKG/NEMO), thereby suppressing downstream signal transduction. The macroautophagy/autophagy receptor OPTN (optineurin) was exploited by NS2 to mediate the selective autophagic degradation. Furthermore, the K72 residue was critical for the NS2-mediated degradation of IKBKG/NEMO, as the K72R substitution in NS2 disrupted the IKBKG/NEMO-NS2 interaction and abrogated the autophagic degradation. In addition, NS2 mutant virus displayed less viral load and milder pathogenicity in mice. In conclusion, these findings highlighted the novel biological function of IAV NS2 in exploiting selective autophagy to evade host defenses, and offered a potential target for controlling IAV infections.: 3-MA: 3-methyladenine; AIV: avian influenza virus; ATG7: autophagy related 7; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CHX: cycloheximide; co-IP: co-immunoprecipitation; CHUK/IKKα: component of inhibitor of nuclear factor kappa B kinase complex; DAPI: 4', 6-diamidino-2-phenylindole, dihydrochloride; dsRNA: double-stranded RNA; dpi: days post-infection; EID: 50% egg infective dose; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; hpi: hours post-infection; IAV: influenza A virus; IFN: interferon; IKBKB/IKKβ: inhibitor of nuclear factor kappa B kinase subunit beta; IFNG: interferon gamma; IKBKG/NEMO: inhibitor of nuclear factor kappa B kinase subunit gamma; IKK: IκB kinase; IP: immunoprecipitation; IRF3: interferon regulatory factor 3; IRF7: interferon regulatory factor 7; LAMP1: lysosome associated membrane protein 1; LIR: LC3-interacting region; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K14/NIK: mitogen-activated protein kinase kinase kinase 14; MAVS: mitochondrial antiviral signaling protein; MLD: 50% mouse lethal dose; MOI: multiplicity of infection; MRV/Sendai virus: murine respirovirus; NBR1: NBR1 autophagy cargo receptor; NEP: nuclear export protein; NFKB/NF-κB: nuclear factor kappa B; NFKB2/p100: nuclear factor kappa B subunit 2; NFKBIA/IκBα: NFK inhibitor alpha; NP: nucleoprotein; NS1: non-structural protein 1; OPTN: optineurin; PB1: basic polymerase 1; PBS: phosphate-buffered saline; poly(I:C): polyriboinosinic polyribocytidylic acid; PRRs: pattern recognition receptors; RELA/p65: RELA proto-oncogene, NF-kB subunit; RELB: RELB proto-oncogene, NF-kB subunit; RIGI: RNA sensor RIG-I; RIGI-IN: RIGI-CARD; RLR: RIGI-like-receptor; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; SIM: SUMO-interacting motif; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; TBK1: TANK binding kinase 1; TNF: tumor necrosis factor; TRAF6: TNF receptor associated factor 6; TOLLIP: toll interacting protein; Vec: empty vector; vRNP: viral ribonucleoprotein. - Source: PubMed
Publication date: 2026/05/27
Zhang BoHan LebinCui ChenyingHuang JiaxinZhu QiyunLei CaoqiXu Shuai - 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