Mouse Monoclonal Antiobody to NCOR1
- Known as:
- Mouse Monoclonal Antiobody NCOR1
- Catalog number:
- mab-606020265
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Antagene
- Gene target:
- Mouse Monoclonal Antiobody NCOR1
Related genes to: Mouse Monoclonal Antiobody to NCOR1
- Gene:
- NCOR1 NIH gene
- Name:
- nuclear receptor corepressor 1
- Previous symbol:
- -
- Synonyms:
- N-CoR, hCIT529I10, TRAC1, hN-CoR, KIAA1047, MGC104216, PPP1R109
- Chromosome:
- 17p12-p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2018-02-13
Related products to: Mouse Monoclonal Antiobody to NCOR1
Related articles to: Mouse Monoclonal Antiobody to NCOR1
- 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 - Osteosarcoma (OS) is characterized by high metastatic potential and marked chemoresistance, with cancer stem cells (CSCs) serving as major drivers of malignant progression. Canine osteosarcoma (cOS) is considered an ideal comparative medicine model for human osteosarcoma (hOS). Accumulating evidence indicates that aberrant glucose metabolism and hexosamine biosynthetic pathway (HBP, hexosamine biosynthetic pathway)/O-linked N-acetylglucosamine (O-GlcNAc)ylation are involved in tumor progression; however, the precise mechanisms by which they regulate stemness in canine osteosarcoma cells remain unclear. In this study, we comprehensively employed glucose gradient culture, untargeted metabolomics, O-GlcNAc-modified proteomics, in vitro gene silencing, and a subcutaneous xenograft model in nude mice. Cellular functional assays revealed that high glucose significantly enhanced malignant phenotypes and stemness properties of canine osteosarcoma cells. Metabolomic analyses confirmed aberrant activation of the HBP in osteosarcoma cells. Further experiments demonstrated that high glucose enhances HBP flux and O-GlcNAcylation in a dose-dependent manner; silencing of glutamine-fructose-6-phosphate transaminase 1 (GFPT1), O-GlcNAc transferase (OGT), and O-GlcNAcase (OGA) verified that both the HBP pathway and O-GlcNAcylation positively regulate malignant biological behaviors and stemness maintenance. In vivo tumorigenesis assays demonstrated that OGT knockdown markedly suppressed osteosarcoma growth. O-GlcNAc-modified proteomics identified transducin-like enhancer of split 3 (TLE3), nuclear receptor corepressor 1 (NCOR1), and neurogenic locus notch homolog protein 2 (NOTCH2) as key differentially modified proteins, predominantly enriched in the Wingless/Integrated (Wnt) and Notch signaling pathways. Collectively, our findings demonstrate that high glucose activates the HBP pathway, elevates global O-GlcNAcylation levels, and modifies TLE3/NCOR1/NOTCH2, thereby promoting stemness maintenance in canine osteosarcoma stem cells. This study provides novel metabolic targets for precision therapy of osteosarcoma. - Source: PubMed
Publication date: 2026/07/28
Wang WeiqianYang BingsongZhang GuangminWang MeimeiSun JunpingLi SiyaoKang HuijieHou QingdianLi PujunFan HonggangSha Jichen - Acute lung injury (ALI) remains a major public health challenge. Although Ophiopogonin D (OPD) possesses well-documented anti-inflammatory activity, its therapeutic efficacy and mechanisms in ALI remain elusive. In this study, we established an ALI model via lipopolysaccharide (LPS) challenge and treated mice with OPD. OPD significantly ameliorated multiple indices of lung injury. Using single-cell RNA sequencing (scRNA-seq), we identified the key cell types and pathways mediating OPD's protective effects. scRNA-seq revealed that OPD primarily corrected the M1/M2 macrophage imbalance. Both in vitro and in vivo, OPD suppressed M1 polarization and, more prominently, promoted the differentiation of Plet1 macrophage, an M2-like subset. Mechanistically, OPD activated peroxisome proliferator-activated receptor gamma (PPARγ) to upregulate placenta-expressed transcript 1 (PLET1) expression; this effect was abolished by PPARγ inhibition. Thermal proteome profiling (TPP) coupled with subsequent validation identified nuclear receptor corepressor 1 (NCOR1) as a direct target of OPD. OPD disrupted the NCOR1-PPARγ interaction. Ncor1 knockdown phenocopied OPD's promotion of Plet1 macrophage differentiation, whereas Ncor1 overexpression completely abrogated these effects. Collectively, OPD directly binds NCOR1 and disrupts the NCOR1-PPARγ interaction, thereby activating PPARγ and inducing Plet1 macrophage differentiation to ameliorate LPS-induced ALI. - Source: PubMed
Publication date: 2026/07/24
Wan QianqianWang YumingMa DehongWang NingPei HuanZhang CongmeiLong YuanWu YueyingFang XixingZhang RongxiuMin FeitianBian YuhongWen WeiboCui Huantian - Chromosomal instability (CIN), a hallmark of malignancy, remains poorly understood in clear cell renal cell carcinoma (ccRCC). Here, we identify spindle and kinetochore-associated protein 3 (SKA3) as a critical regulator of CIN in ccRCC. BAP1 loss-of-function mutations, prevalent in ccRCC, drive aberrant SKA3 overexpression. Mechanistically, BAP1 deubiquitinates nuclear receptor co-repressor 1 (NCOR1) to enhance its recruitment to the SKA3 promoter, thereby repressing SKA3 transcription. Additionally, BAP1-mediated histone H2AK119 deubiquitination at the TRIM25 promoter activates the expression of TRIM25, facilitating ubiquitin-proteasome-mediated degradation of SKA3. BAP1 deficiency disrupts both regulatory pathways, leading to aberrant accumulation of SKA3, which fuels CIN and correlates with metastasis progression and poor prognosis. In conclusion, our findings establish dysfunction of the BAP1-SKA3 axis as a molecular driver of CIN in ccRCC and suggest SKA3 as a potential therapeutic target for BAP1-mutant ccRCC. - Source: PubMed
Publication date: 2026/07/15
Wang YueyangLai ChongWang LinglingDeng JingwenTian ZhouLiang ZhiyongZhang Honghe - Ovarian senescence is the fundamental cause of reduced fertility in female animals,however, the molecular characteristics of ovarian ageing in sheep remain insufficiently defined. In this study, ovarian tissues were collected from 12 Qira Black sheep and assigned to group D (1-2 years, = 6) and group H (5-6 years, = 6) for LC-MS/MS-based proteomic profiling. A total of 458 differentially expressed proteins (DEPs) were identified between the two groups, including 211 upregulated and 247 downregulated proteins. Functional enrichment analyses indicated that these DEPs were mainly involved in cell-cycle regulation, oocyte maturation, amino acid metabolism, and inflammation-related signalling pathways, with the Rat Sarcoma(Ras) and Mitogen-Activated Protein Kinase Pathway(MAPK) signalling pathways showing particularly strong enrichment. Protein-protein interaction (PPI) network analysis revealed close interactions among Intraflagellar transport 80(IFT80), Insulin receptor(INSR), Angiopoietin-like 4(ANGPTL4), Receptor interacting serine/threonine kinase 3(RIPK3), Nuclear receptor corepressor 1(NCOR1), and Fms-Related Tyrosine Kinase 4(FLT4), with Insulin receptor(INSR) occupying a central hub position. Collectively, this study establishes a differential proteomic atlas of ovarian ageing in Qira Black sheep, highlights the potential importance of Rat Sarcoma(Ras) and Mitogen-Activated Protein Kinase Pathway(MAPK) signalling in this process, and identifies Insulin receptor(INSR) as a candidate target, thereby providing a theoretical basis for subsequent mechanistic studies and the development of molecular markers. - Source: PubMed
Publication date: 2026/06/30
Guo PeilinPei LinlinLiu NingjieWang WenhaoQiao AndiXu XinLiu Chunjie