NCOR1 antibody Host rabbit
- Known as:
- NCOR1 (anti-) Host host: rabbit
- Catalog number:
- 'C0358-2
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- NCOR1 antibody Host rabbit
Related genes to: NCOR1 antibody Host rabbit
- 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 Host rabbit
Related articles to: NCOR1 antibody Host rabbit
- Nuclear receptor corepressor 1 (NCoR1) and silencing mediator of retinoic acid and thyroid hormone (SMRT) are critical regulators that mediate transcriptional repression through histone deacetylation. Despite high structural homology, their distinct roles in the central nervous system remain poorly understood. To elucidate these roles, we generated neuronal-specific NCoR1 or SMRT knockout mice using Snap25-IRES2-Cre mice. Behavioral assessments revealed that while both NCoR1 and SMRT deficiency led to hypoactivity, social deficits, and mild anxiety, NCoR1-deficient mice uniquely exhibited enhanced learning abilities in a visual discrimination task, indicating functional separation in cognitive regulation. This divergence was supported by RNA-sequencing in the amygdala at postnatal day 21 (PND 21), where SMRT deletion upregulated 449 genes, whereas NCoR1 deletion upregulated only 8 genes. Furthermore, we investigated the protein stability of HDAC3, the primary enzymatic partner of these corepressors. At PND 21, HDAC3 levels were significantly reduced in the NCoR1-deficient hippocampus but significantly increased in the SMRT-deficient amygdala. In contrast, HDAC3 levels remained stable in the adult cerebellum and PND 3 cerebrum regardless of corepressor status. Notably, while mice with deletion of both NCoR1 and SMRT exhibit early postnatal lethality, their HDAC3 levels were unchanged compared to controls at PND 3, suggesting that the lethal phenotype is not primarily driven by a systemic loss of HDAC3 protein. Collectively, our findings demonstrate that NCoR1 and SMRT function through independent transcriptional networks and context-dependent regulatory mechanisms. This study highlights the specialized, non-redundant roles of these homologous corepressors in the brain according to developmental stage and region. - Source: PubMed
Publication date: 2026/06/10
Amano IzukiRitter Megan JNinomiya AyaneKawabata-Iwakawa ReikaVierling TaylorCespedes Isabella SalgueroHollenberg Anthony NKoibuchi Noriyuki - How the small intestine ages at the cellular and molecular level has been unclear. Here we profile single nuclei from young and aged primate small intestine and find that aging brings barrier dysfunction, chronic inflammation and a shift in stem cell differentiation away from absorptive cells toward secretory cells. Through integrative multimodal analysis, we identify the transcriptional corepressor NCoR1 as a key player whose decline is conserved in the aging human gut. In human intestinal epithelial cells and organoids, knocking down NCOR1 recapitulates aging phenotypes including senescence, disrupted junctions and lineage imbalance, whereas overexpressing NCoR1 alleviates them. Metformin-a geroprotective drug-restores NCoR1 levels and delays intestinal aging in nonhuman primates. Our work points to NCoR1 as a central regulator of small intestinal aging and suggests a pharmacologically actionable strategy to counter age-related intestinal decline. - Source: PubMed
Publication date: 2026/06/09
Li JingyiLu XiaoyongTong TianhongZhou XinZhang BaohuSun XiaoyanZhao BingXu GangYang JinjiangFan YanlingHu JianliYan HaotengJi ZhejunLi MinghengChe ShanshanYang YuanhanDing YingjieWang QiaoranSun ShuhuiMa ShuaiWang SiIzpisua Belmonte Juan CarlosQu JingZhang WeiqiLiu Guang-Hui - To enhance risk stratification in metastatic castrate-resistant prostate cancer (mCRPC), we developed clinical and integrated clinico-genomic prognostic nomograms combining clinical prognostic factors with copy number alteration-based risk scores (RSs) in circulating tumor DNA (ctDNA) and metastatic tissue to predict 1-, 2-, and 3-year overall survival (OS) probabilities. - Source: PubMed
Kohli ManishShankar AnushkaLloyd JenniferWang LiangHuo XingyueFadlullah Muhammad ZakiTan Aik ChoonFinkelstein Joseph - Anxiety disorders are prevalent and can greatly impact well-being. The biological mechanisms behind anxiety are not fully understood, but growing evidence suggests a role for DNA methylation. Here, we conduct a large-scale methylome-wide association study of lifetime anxiety in 14,443 participants (1817 cases and 12,626 controls) in whole blood, and, through epigenomic deconvolution, 12 different blood cell types. We detect four CpG associations at methylome-wide significance in whole blood, and a range between 15 and 124 associations among the cell types. Top cell type-specific findings include genes potentially involved in stress response such as FAM171A2 and VIPAS39 and genes that have been previously linked to anxiety, such as NCOR1. Whole blood and all cell type-specific findings significantly overlap with findings from two previous methylome-wide association studies of lifetime anxiety and an anxiety GWAS, suggesting results are robust. Pathway analyses broadly implicate anxiety-related impacts on cellular stress response. Analyses of five epigenetic clocks suggest DNA methylation-based phenotypic aging and pace of aging may be accelerated in anxiety. Our results support a cell type-specific relationship between DNA methylation and anxiety and highlight the utility of including cell type-specific analyses in whole blood studies of DNA methylation. - Source: PubMed
Publication date: 2026/06/01
Ingram Sarah JRamachandruni SrimannCarreras-Gallo NataliaDwaraka Varun BSmith RyanHettema John Mvan den Oord Edwin J C GClark Shaunna L - Smooth muscle nuclear receptor corepressor 1 (NCOR1) is implicated in phenotype modulation and aortic aneurysms, but its role in blood pressure regulation remains unclear. In the present study, using smooth muscle NCOR1 knockout male mice in combination with an angiotensin II-induced hypertensive mouse model, we found that NCOR1 deficiency reduced blood pressure and attenuated vascular remodeling. NCOR1 deficiency also alleviated age-related hypertension in aged male mice. Using inducible NCOR1-knockout male mice, we found that the deletion of smooth muscle NCOR1 prevents further exacerbation of hypertension. Compared with control VSMCs, NCOR1 deficient-vascular smooth muscle cells (VSMCs) exhibited less proliferation, migration, and contraction. Mechanistically, NCOR1 deficiency downregulated the expression of adhesion-related genes and impaired integrin signaling pathway in VSMCs. Collectively, our results indicate that NCOR1 regulates the expression of integrins in VSMCs, controls the proliferation, migration, and contraction of VSMCs, and finally affects blood pressure and vascular remodeling in male mice. - Source: PubMed
Publication date: 2026/05/11
Du Lin-JuanMeng Xiao-QianXu ShuoLiu YanZhou Lu-JunZhang Wu-ChangDuan Sheng-Zhong