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
- Feed efficiency (FE) is a complex trait which determines livestock production profitability, yet the molecular mechanisms behind it remain unclear. This study investigated the blood transcriptomic profile of lambs, alongside genotype data with the aim to uncover the genetic basis of FE traits such as absolute dry matter intake (DMI), DMI adjusted for body size (DMI), average daily live weight gain (ADG), and residual feed intake (RFI). - Source: PubMed
Publication date: 2026/08/21
Chacko Kaitholil Steffimol RoseMooney Mark HCristobal-Carballo OmarHosseinzadeh SevdaRezwan Faisal IAubry AurélieShirali Masoud - Cardiac hypertrophy is a major contributor to heart failure development, making its prevention and treatment critical for reducing heart failure-associated mortality. Although alternative splicing is recognized as a key regulatory mechanism in myocardial hypertrophy, the precise pathways involved remain incompletely defined. - Source: PubMed
Publication date: 2026/09/02
Shi YuanqiSheng SiqiWang BinLv PengchengLiu JialiangDong PengweiZhang JingyueChen JiulingZhang HaiyuLv LinYang JialeLuo DankunLi YueDong Zengxiang - Interferon (IFN) signaling plays a pivotal role in orchestrating antitumor immunity and shaping the response to immune checkpoint blockade (ICB). Although genetic alterations that impair the IFN pathway have been reported, such events are relatively rare, suggesting a potential contribution of epigenetic dysregulation. Here, we identified a RUNX2-mediated epigenetic mechanism that disrupts the type I interferon (IFN-I) signaling pathway in osteosarcoma (OS), thereby limiting the efficacy of ICB. Development of an algorithm to assess the association of 1,425 transcription factors with IFN pathway activation in human OS tumors enabled identification of RUNX2 as a potential negative regulator of IFN signaling. RUNX2 depletion in OS cells activated the IFNB1-driven IFN-I response. Mechanistically, RUNX2 formed a transcriptional repressor complex with NCOR1 and HDAC3 that reduced H3K9 acetylation at the enhancers of key IFN-I genes, leading to their downregulation. Inhibition of the RUNX2-NCOR1-HDAC3 complex enhanced IFN-I signaling, with cGAS, STING, and IFNB1 being required for the induction of interferon-stimulated genes and tumor suppression. Paradoxically, reactivation of IFN-I signaling also upregulated immune checkpoint molecules PD-L1 and PD-L2. Combination treatment with a selective HDAC3 inhibitor and anti-PD-1 antibody led to durable tumor regression in syngeneic OS mouse models, accompanied by increased cytotoxic T cell infiltration. These findings reveal a mechanistic link between RUNX2-driven epigenetic repression and impaired antitumor immunity via the cGAS-STING-IFN-I axis and suggest a rational combinatorial strategy to overcome OS resistance to ICB. - Source: PubMed
Publication date: 2026/09/01
Wang ShashaYan HualongMondal PayelAyaz GamzeYang Howard HKim Young-ImTran Andy DKruhlak Michael Jdu Bois WendyLee Maxwell PHuang Jing - 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