AIB1 Monoclonal Antibody [50B6]
- Known as:
- AIB1 Monoclonal Antibody [50B6]
- Catalog number:
- a-0424-100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Epigentek inc
- Gene target:
- AIB1 Monoclonal Antibody [50B6]
Related genes to: AIB1 Monoclonal Antibody [50B6]
- Gene:
- NCOA3 NIH gene
- Name:
- nuclear receptor coactivator 3
- Previous symbol:
- -
- Synonyms:
- RAC3, AIB1, ACTR, p/CIP, TRAM-1, CAGH16, TNRC16, KAT13B, bHLHe42, SRC-3, SRC3
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2016-10-05
Related products to: AIB1 Monoclonal Antibody [50B6]
Related articles to: AIB1 Monoclonal Antibody [50B6]
- Approximately 60% of patients with ulcerative colitis (UC) show steroid resistance or dependence, underscoring the need for biomarkers predicting therapeutic response. Despite increasing availability of biologics, corticosteroids remain essential first-line therapy for moderate-to-severe flares in many settings. We applied an integrative systems biology and machine-learning framework to combine microRNA (miR) and mRNA expression profiles from matched rectal biopsies and plasma samples of UC patients treated with corticosteroids, aiming at exploring classification potential of such biological data. Transcriptomic mRNA and miR profiling was performed at baseline and after three days of therapy, and patients were classified as responders or non-responders after seven days. Differential expression results were embedded into a previously defined curated molecular network-based mathematical model of the mechanism of action (MoA) of glucocorticoid signaling over UC to enhance biological interpretability. miR-mRNA interactions were prioritized based on database support and relevance to glucocorticoid receptor and inflammatory signaling as defined in the molecular mathematical model. Key transcriptional co-regulators within this network, including NCOA3, CBP, NCOR1, and NRIP1, distinguished response groups, together with miRs such as miR-145-5p, miR-10b-5p, and miR-16-5p. Several miR candidates showed circulating-tissue consistency and conserved behavior in a TNBS-induced colitis mouse model, in terms of expression in response to corticoids and miR-mRNA inverse correlations. This study proposes a mechanistically grounded framework for corticosteroid response biomarker discovery; however, findings are exploratory and prospective validation in independent cohorts is required before clinical applicability can be established. - Source: PubMed
Publication date: 2026/08/03
Ginés IrisSuau RogerNaves Juan EnriqueBernal CarlaClua LauraLorén VioletaPluvinet RaquelMonfort-Ferré DiandraLópez Balastegui MartaSánchez Herrero José FranciscoSegú-Vergés CristinaAransay Ana MariaBuschbeck MarcusMañosa MíriamSumoy LauroSerena CarolinaDomènech EugeniManyé Josep - Nuclear receptor coactivator 3 (NCOA3) is associated with various cancers, but its function and mechanism in glioblastoma multiforme (GBM) are still unclear. Bioinformatics analysis, in vitro cell experiments (NCOA3 silencing (si-NCOA3) or NCOA3 small-molecule inhibitor SI-2), in vivo animal models, and metabolic level detection were used to elucidate the activity of NCOA3 in GBM. The data revealed that GBM tissues had NCOA3 overexpression, which was linked with poor prognosis. It regulates pathways related to glycolysis, the cell cycle, and immunosuppression. Functionally, si-NCOA3/SI-2 suppressed GBM cell proliferation and migration. In vivo, sh-NCOA3/SI-2 demonstrated anti-glioma effects. Metabolically, treatment with si-NCOA3/SI-2 reduced glucose uptake, pyruvate and lactate production, ATP levels, and glycolysis-related enzyme expression in GBM cells. Combination therapy with SI-2 and TMZ enhanced GBM cell sensitivity to TMZ. Single-cell RNA sequencing revealed high NCOA3 expression in glioma stem cells (GSCs). si-NCOA3 inhibited GSCs proliferation and self-renewal while reducing the expression of Nestin and SOX2. NCOA3 is an oncogene in GBM. In mechanism, NCOA3 promotes GBM progression by enhancing the Warburg effect. In addition, NCOA3 is also highly expressed in GSCs and significantly promotes their proliferation and self-renewal ability. NCOA3 may represent a promising therapeutic target for GBM. - Source: PubMed
Publication date: 2026/08/13
Luo QianYang JiayingYin HailinYang MeiLiang YueyangHou YixuanSun XinzeLiu JixuanZhang Ling - Staphylococcus aureus is a major opportunistic pathogen in humans; airborne exposure to this bacterium is associated with increased respiratory disease incidence. The airway epithelium, serving as the primary barrier against inhaled pathogens, is particularly vulnerable to bacterial invasion. However, the underlying mechanisms and relevant biomarkers for this exposure remain underexplored. In this study, we evaluated the toxic effect mechanisms and biomarkers of S. aureus aerosol exposure to human bronchial epithelial (16HBE) cells at the air-liquid interface using microRNA (miRNA) sequencing. We found that exposure to aerosols containing 3.21 × 10 to 6.54 × 10 CFU/mS. aureus impaired cell viability and proliferation, induced mitochondrial damage, and triggered inflammation by upregulating IFN-γ expression. The bacterium secreted pore-forming toxins, coagulases, nucleases, enterotoxins, and β-hemolysins to lyse cells and induced a cytokine storm by modulating the expression of hla, coa, nuc, sea, and hlb genes. 16HBE cells primarily upregulated Toll-like receptors (TLR1 and TLR5), mucins (MUC1), and epidermal growth factor receptors (KGF7 and TEP1) to recognize invasion, activate the immune response, and protect the cell membrane. miRNA sequencing suggested that medium-concentration exposure induced more differentially expressed genes (DEGs), particularly downregulated DEGs, than other concentrations. Twelve miRNAs uniquely shared across the exposure groups were considered potential biomarkers of S. aureus aerosol exposure. Regulatory networks analysis showed that miR-19a-3p, miR-18a-5p, miR-106b-5p, and miR-142-5p could influence cancer-related pathways and the MAPK signaling pathway by targeting genes such as CRK, NCOA3, MAPK1, and TGFR2 and may serve as biomarkers of 16HBE cell damage. Overall, this study elucidates the injury mechanisms and potential biomarkers of S. aureus aerosol exposure in respiratory cells, advances the understanding of airborne pathogen-induced toxicity. - Source: PubMed
Publication date: 2026/07/15
Liang ZhishuWu YanranNi JiashengYang YunlingHuang SiminJiang XiaofengBi Xinhui - The pregnane X receptor (PXR) is a nuclear receptor that regulates the expression of drug-metabolizing enzymes in response to various chemicals. Ligand binding to PXR induces a conformational alteration of the C-terminal coactivator-binding motif activation function 2 (AF2), leading to the recruitment of coactivators. The contribution of each coactivator to PXR-mediated transcription may vary depending on the ligand. Therefore, identifying ligand-dependent differences in coactivator recruitment is important for understanding the biological functions of PXR. In this study, we investigated the ligand-dependent recruitment of coactivators using a PXR mutant containing a three-alanine insertion immediately upstream of AF2 (PXR-3A). Mammalian two-hybrid assays showed that PXR-3A recruited coactivators in a ligand-dependent manner. Treatment with the PXR ligand SR12813 induced the interaction of PXR-3A with coactivator peptides. Using reporter assays with the PXR-binding motifs from CYP3A4, CYP2C19, and CYP2C9 promoters, we evaluated the influences of coactivator overexpression on ligand-dependent reporter activity. In assays with the CYP3A4 promoter, rifampicin, rifaximin, or SR12813 induced reporter activity, and overexpression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC1α) or nuclear receptor coactivator 1 (NCoA1) enhanced rifaximin- and SR12813-dependent transactivation. In assays using the CYP2C19 promoter, rifampicin and rifaximin induced reporter activity, whereas SR12813 did not. PGC1α enhanced rifaximin- or SR12813-induced transcription, whereas NCoA1, NCoA2, and activating signal cointegrator-2 (ASC2) did not exhibit clear ligand-dependent effects. NCoA3 knockdown in HepaRG cells attenuated SR12813-dependent induction of CYP2C19. Taken together, using the PXR-3A mutant, we demonstrated ligand-dependent recruitment of coactivators by PXR. - Source: PubMed
Sugawara AyakaShizu RyotaNishiguchi HikaruMotokatsu KotonaHosaka TakuomiSasaki TakamitsuYoshinari Kouichi - Most autoimmune disease-associated variants lie in non-coding regions, but the molecular mechanisms linking these variants to gene regulation remain poorly understood. A major unresolved challenge is to determine how disease alleles alter transcription factor (TF) binding, cofactor (COF) recruitment, and enhancer activity at scale. Here, we used the CASCADE method to profile differential binding of five TFs and ten COFs to 2,901 autoimmune disease-associated variants in Jurkat T cells, identifying 516 binding-modulating variants. Variants impacting binding were enriched among MPRA-defined expression-modulating variants and were strongly concordant with allele-specific reporter expression, linking altered TF/COF recruitment to enhancer activity. A majority of variants perturb binding of five major TF families - ETS, RUNX, SP/KLF, OVOL/MYBL, and bHLH - all of which have established roles in T cell biology. Notably, we find that ETS and RUNX factor binding is enriched at different variant functional classes, suggesting that they act through distinct regulatory mechanisms at disease loci. We describe allele-dependent regulator "switching" at several loci, where distinct complexes are found at reference and variants alleles, and we identify a recurrent regulatory module involving FOXM1 and the cofactors TIP60, BRD4, NCOA3, and NCOA1 assembling on ETS sites that tracks with gene expression. Together, this integrated biochemical and functional framework prioritizes autoimmune disease-associated variants by linking allele-specific TF/COF binding mechanisms to enhancer activity. - Source: PubMed
Publication date: 2026/05/22
Dashtiahangar MaryamSiggers Trevor