RELB & RELA Protein Protein Interaction Antibody Pair
- Known as:
- RELB & RELA Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0617
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- RELB & RELA Protein Interaction Antibody Pair
Related genes to: RELB & RELA Protein Protein Interaction Antibody Pair
- Gene:
- RELA NIH gene
- Name:
- RELA proto-oncogene, NF-kB subunit
- Previous symbol:
- NFKB3
- Synonyms:
- p65
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2016-10-05
- 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 & RELA Protein Protein Interaction Antibody Pair
Related articles to: RELB & RELA Protein Protein Interaction Antibody Pair
- 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 - 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 - Breast cancer remains the second leading cause of cancer-related mortality among women, with triple-negative breast cancer (TNBC) exhibiting a particularly poor five-year prognosis. Here, we demonstrated that, among genetic and pharmacological perturbations targeting DNA replication, suppression of DNA polymerase epsilon (POLE) induced a potent, TNBC-specific gene expression signature enriched in inflammatory cytokines that are transcriptional targets of NF-κB. TNBC cells exhibited markedly higher levels of DNA damage and canonical NF-κB activation compared to luminal breast cancer cells. Notably, NF-κB activation in this context depended on the canonical component RELA but not the non-canonical component RELB. Mechanistically, ATM, STING, and RIG-I each contributed to NF-κB activation following POLE suppression. POLE suppression in an in vivo murine TNBC model led to cancer cell-intrinsic elimination of tumor burden and increased immune cell infiltration. Together, these findings support a model in which replication stress from POLE inhibition triggers robust NF-κB-mediated inflammation and immune microenvironment remodeling in TNBC and can independently trigger tumor eradication. These results suggest a potential therapeutic avenue for targeting POLE in TNBC. - Source: PubMed
Publication date: 2026/04/21
Sher Elizabeth FFujihara Kenji MTao AnthonySastourne-Haletou PaulErenburg DianaSviderskiy Vladislav OMir HannanKarakousi TriantafylliaLoomis Cynthia ADeng JiehuiRuggles Kelly VWong Kwok-KinPossemato Richard - The nuclear factor kappa B (NF-κB) signaling pathway plays an indispensable role in defending against bacterial infections. However, the complete repertoire of its core components-NF-κB transcription factors, IκB inhibitors, the canonical IKK complex, and IKK-related kinases-remains unclear in most teleosts. In this study, we conducted a genome-wide analysis of grass carp (Ctenopharyngodon idella) and systematically identified five NF-κB family members (RelA and NF-κB1 as core canonical effectors; RelB and NF-κB2 as non-canonical effectors; plus c-Rel), seven inhibitor of NF-κB (IκB) members (including the classical inhibitor IκBα with two subtypes: IκBαa and IκBαb, as well as IκBβ, IκBNS, IκBζ, IκBε, and Bcl-3), three components of the canonical IKK complex (IKKα, IKKβ, and IKKγ/NEMO), and two IKK-related kinases (TBK1 and IKKε). These genes are distributed across 13 chromosomes. Synteny analysis revealed that the chromosomal arrangement of these three gene complexes is highly conserved in cyprinids. Both sequence and phylogenetic analyses demonstrated that the members within each complex are highly conserved. Transcriptomic data revealed that members of the NF-κB, IκB, canonical IKK complex, and IKK-related kinase are widely expressed in various tissues, with NF-κB2, IκBαa, IκBαb, and TBK1 exhibiting relatively high basal expression levels across tissues and actively responding to bacterial and viral challenges. qRT-PCR analysis further confirmed that the expression of most members changed significantly in the spleen and head kidney of grass carp following infection with grass carp reovirus (GCRV-II) or Aeromonas hydrophila. In conclusion, this comprehensive and systematic analyses on NF-κB, IκB, the canonical IKK complex, and IKK-related kinases establishes a crucial molecular foundation for subsequent functional research on the NF-κB and interferon-associated signaling pathways in teleost. - Source: PubMed
Publication date: 2026/03/27
Lv MaolinChen GuanyuLi WenxingLu YizhongTang BoSu Jianguo - NF-κB signaling can be subdivided into canonical and noncanonical pathways, culminating in the transcriptional activity of RELA and RELB, respectively. However, the upstream signals that activate these transcription factors and their specific regulatory roles in pancreatic ductal adenocarcinoma (PDAC) remain incompletely understood. We investigated the differential activation and function of RELA and RELB in PDAC using transcriptome-wide gene expression profiling, genome-wide occupancy mapping, and epigenomic analysis. Temporal activation patterns were assessed following TNFα or TWEAK stimulation. Single-cell RNA sequencing and multiplex immunofluorescence staining were used to characterize activity in primary PDAC tissues. Motif enrichment and chromatin accessibility were evaluated to determine transcription factor binding dynamics and co-regulatory associations. We demonstrate that TNFα is the primary activator of canonical NF-κB signaling via RELA, while TWEAK selectively engages noncanonical signaling through RELB in PDAC. RELA and RELB display distinct temporal dynamics and regulatory activity. RELA binds to both open and closed chromatin and drives a broad transcriptional program, while RELB exclusively occupies pre-accessible chromatin regions co-enriched for AP1 motifs. Motif analysis reveals a particularly strong association of RELB with AP1 elements, suggesting selective co-regulation. Single-cell transcriptomic analysis and multiplex staining in primary tumors reveal distinct spatial and cellular distribution patterns, with RELA and RELB active in separate tumor and microenvironmental compartments. These findings underscore the distinct and complementary roles of TNFα and TWEAK in regulating NF-κB signaling in PDAC. TNFα engages a broader transcriptional program via RELA, whereas TWEAK targets a more selective set of genes marked by chromatin accessibility and AP1 co-binding through RELB. This study provides critical insight into the regulatory dynamics of NF-κB signaling in pancreatic cancer and highlights the specialized functions of RELA and RELB in modulating gene expression and tumor-microenvironment interactions. - Source: PubMed
Publication date: 2026/03/17
Aggrey-Fynn Joana EBusch JoshuaSaul DominikRajput AshishWillecke KerstinManjunath MeghanaKlimt NicoleRajendran KothaiSchacherer NadineGe WanwanThiel JuliaAbdelrahman AmroTruty Mark JDong MengJohnsen Steven A