Ask about this productRelated genes to: NCOR1 antibody
- 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 antibody
Related articles to: NCOR1 antibody
- Endometriosis-associated infertility is a complex condition in which the presence of endometrial-like tissue disrupts implantation and early pregnancy. Epigenetic regulators are critical for implantation and decidualization, yet their contribution to endometriosis-associated infertility remains incompletely understood. Nuclear receptor corepressor 1 (NCOR1), an epigenetic coregulator of steroid hormone signaling, has an incompletely defined role in endometriosis and early pregnancy. We show that NCOR1 expression is significantly reduced in the eutopic endometrium of infertile women with endometriosis. Using a conditional uterine -knockout mouse model ( ), we demonstrate that NCOR1 loss is associated with increased ectopic lesion burden, implantation failure, defective decidualization, and severe subfertility, despite normal ovarian hormone production. NCOR1 deficiency was associated with disrupted progesterone-responsive signaling and endometrial receptivity. Together, these findings identify NCOR1 as an important regulator of endometrial function during early pregnancy and support an association between reduced NCOR1 expression and endometriosis-associated infertility. - Source: PubMed
Publication date: 2026/04/12
Nguyen Loan Thi KimTran Dinh NamAuwerx JohanKumar Harini RaghuYoung Steven LLessey Bruce AArora RiplaYoo Jung-YoonKim Tae HoonJeong Jae-Wook - Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver disorder with limited treatment and manifests as hepatic lipid accumulation. The reduction of nuclear receptor corepressor 1 (NCoR1) activates the nuclear receptor PPARα, which plays a crucial role in alleviating lipid accumulation. We found that Scutellarin (Scu) regulated autophagy-mediated NCoR1/PPARα to enhance fatty acid (FA) β-oxidation and peroxisome production, thereby alleviating the lipid accumulation of MASLD. We used palmitic acid (PA)-treated human hepatocellular carcinoma (HepG2) and alpha mouse liver 12 (AML12) cells, as well as high-fat diet-fed C57BL/6J mice to evaluate the protective effect of Scu on MASLD. Scu reduced the levels of total cholesterol, triglycerides, and lipid droplets, whereas it dose-dependently increased the levels of β-hydroxybutyrate. In addition, Scu increased mRNA and protein expression of PPARα and promoted the transcriptional activity of FA β-oxidation-related target genes. In vitro, inhibition of PPARα with small interfering RNA (siRNA) abolished the activation of FA β-oxidation by Scu. Cellular thermal shift assay and drug affinity responsive target stability demonstrated that Scu did not interact directly with PPARα. Moreover, Scu increased the protein expression of 70-kDa peroxisomal membrane protein and the mRNA expression of peroxisome biogenesis-related genes. These effects were reversed by PPARα-siRNA. Scu improved the impaired autophagy while reducing the mRNA and protein expression of NCoR1. Notably, Scu reduced the colocalization of NCoR1 with PPARα and increased its colocalization with the autophagosome GABARAP. 3-MA, an autophagy inhibitor, attenuated Scu-mediated protective effects by FA β-oxidation and peroxisome biogenesis both in vitro and in vivo. In summary, Scu reduces lipid accumulation by improving the impaired autophagy, decreasing NCoR1 expression to activate PPARα, thereby simultaneously enhancing FA β-oxidation and peroxisome biogenesis, ultimately ameliorating hepatic steatosis. - Source: PubMed
Publication date: 2026/05/05
Zheng JianmeiCheng LuWei YingminRen MingshiWang LeiWang JingwenZhou WuliuHuang HuiWu Feihua - : Nuclear receptor corepressors NCOR1 and NCOR2 are key regulators of transcriptional repression, chromatin remodelling, and immunometabolic signalling. While NCOR1 has already been linked to vascular biology, its relevance in abdominal aortic aneurysm (AAA) remains unclear, particularly for NCOR2. This study aimed to investigate the expression, cellular localisation, and molecular interactions of NCOR1/2 in human AAA tissue. : Human AAA samples (elective and ruptured) ( = 45) and non-aneurysmal control aortas ( = 18) were obtained from our Swiss Vascular Biobank. Transcriptomic profiling was performed using ribosomal RNA-depleted RNA sequencing. Differential expression and correlation analyses were performed using DESeq2/EdgeR and Spearman rank correlation with Benjamini-Hochberg correction. Cellular localisation was assessed through immunohistochemistry (IHC). : Bulk transcriptomic analyses showed no significant differences in NCOR1 or NCOR2 expression between AAA and controls. IHC revealed that NCOR1 was found in endothelial cells (ECs), smooth muscle cells (SMCs), and inflammatory infiltrates, while NCOR2 was primarily associated with macrophages. Correlation analyses suggest that NCOR1 interacts with various cellular markers, proteolytic enzymes, inflammatory mediators, and epigenetic regulators, including the lncRNA MALAT1. NCOR2 showed distinct associations with remodelling enzymes, TGFB1 signalling, selective epigenetic modifiers, and lncRNA H19. : The lack of transcriptional differences in NCOR1 and NCOR2 between AAA and controls does not exclude cell-type-specific regulation or functional relevance. The specific cellular distributions and molecular associations in human AAA imply that NCOR1 and NCOR2 play non-redundant roles in vascular remodelling, inflammation, and epigenetic regulation. Our findings highlight NCOR pathways as potential modulators of AAA pathophysiology and promising targets for future therapies. - Source: PubMed
Publication date: 2026/04/16
Pelisek JaroslavYundung YankeyMenges Anna-LeonieRössler FabianReutersberg BenediktZimmermann AlexanderGeiger Martin - MicroRNA and mRNA profiling of T cells from Acquired Aplastic Anaemia (AA) patients using both in-silico and in-vitro methods identified molecular changes, including altered immune-regulatory gene expression, linked to T-cell dysregulation and AA pathobiology. - Source: PubMed
Publication date: 2026/04/16
Rai BhuvneshSabereen GhazalaSaxena PragatiSrivastava JyotikaGupta RuchiChaturvedi Chandra Prakash - Metabolic bone disease (MBD) is a multifactorial condition that leads to microarchitectural and bone mass disturbance. The association and mechanisms between MBD and hypothyroidism are not comprehensively elucidated. Moreover, long non-coding RNAs (lncRNAs), as critical regulators in biological processes, are one category of RNAs that could regulate gene expression through various mechanisms. - Source: PubMed
Publication date: 2026/02/14
Bakhti MaliheTaghian FarzanehJalali Dehkordi KhosroMirsafaei Rizi Rezvan