NCOR1 Pre-design Chimera RNAi
- Known as:
- NCOR1 Pre-design Chimera RNAi
- Catalog number:
- H00009611-R01
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- NCOR1 Pre-design Chimera RNAi
Related genes to: NCOR1 Pre-design Chimera RNAi
- 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: NCOR1 Pre-design Chimera RNAi
Related articles to: NCOR1 Pre-design Chimera RNAi
- 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 - Genomic complexity and small case numbers make statistically robust assessment of mutational patterns in osteosarcoma difficult. The authors analyzed a large cohort of targeted next-generation sequencing data from osteosarcoma cases from young patients submitted for clinical testing to Foundation Medicine. - Source: PubMed
Bousquet Hannah GKuang ZhengVega Lorena Lazo de laCeca EvelinaSchiantarelli JuliaHonecker JuliusHiemenz Matthew CForrest Suzanne JJaneway Katherine A - Hepatocellular carcinoma (HCC) remains a therapeutic challenge due to the limited efficacy of current systemic therapies. To identify potential therapeutic approaches, computational analysis of HCC datasets and drug screening were integrated, leading to the repurposing of hematological malignancy drug selinexor (an XPO1 inhibitor) for HCC treatment. Functional studies revealed that XPO1 inhibition triggers oxidative stress and cell cycle arrest in HCC cells through nuclear sequestration of NCOR1, disrupting redox homeostasis through FOXK1-dependent transcriptional activation of genes associated with reactive oxygen species (ROS). A genome-wide CRISPR-Cas9 screen further identified the KEAP1-NRF2 axis as a key determinant of sensitivity to XPO1 inhibition. Furthermore, high-throughput compound screening demonstrated that disulfiram, a clinically used aldehyde dehydrogenase inhibitor, synergizes with XPO1 inhibitor through exacerbation of ROS accumulation. Collectively, these findings demonstrate the therapeutic repurposing of selinexor for HCC while uncovering its mechanism of action, establishing a predictive biomarker, and proposing an immediately translatable combination therapy. - Source: PubMed
Publication date: 2026/07/07
Wang WeiZhang LinmengZuo QiaozhuMa XuhuiCao YingZhu LiliJi ShuyiQin WenxinWang HuiYuan ShengxianBernards RenéWang Cun