NCOR1 (Human) Recombinant Protein (Q01)
- Known as:
- NCOR1 (Human) Recombinant Protein (Q01)
- Catalog number:
- H00009611-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- NCOR1 (Human) Recombinant Protein (Q01)
Related genes to: NCOR1 (Human) Recombinant Protein (Q01)
- 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 (Human) Recombinant Protein (Q01)
Related articles to: NCOR1 (Human) Recombinant Protein (Q01)
- Lagopsis supina is a traditional Chinese medicinal herb used for activating blood circulation and nourishing the blood. This study aims to investigate the pro-angiogenic constituents of L. supina and their mechanisms of their action. 30 compounds derived from the active fraction LS-D (L. supina 60% ethanol-water extract) were screened, of which 15 showed angiogenesis-promoting activity, were screened in a PTK787-induced vascular injury zebrafish model. The active constituents were primarily phenolic acids and phenylpropanoids, among which compounds LS21 (vanillic acid) and LS22 (syringic acid) exhibited the most potent pro-angiogenic effects. These constituents (LS21 and LS22) were selected for further investigation of mechanisms of promoting angiogenesis. Transcriptomic analysis followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment revealed differentially expressed genes and predicted involved pathways. Molecular docking simulated interactions between compounds and key pathway proteins, and RT-qPCR validated gene expression patterns. Mechanistic studies integrating transcriptomics, molecular docking, and RT-qPCR revealed that both LS21 and LS22 downregulated immune-related cell adhesion molecules, while upregulating cdh5 and pecam1a. Additionally, LS21 specifically downregulated the signaling molecules smad2 and smad3a, and upregulated the transcriptional corepressors skila and ncor1. In contrast, LS22 downregulated extracellular matrix-related adhesion molecules and itga2b, while upregulating thbs1a and integrin itgb3b. In conclusion, the L. supina constituents LS21 and LS22 that are primarily phenolic acids and phenylpropanoids, exert their angiogenesis-promoting effects mainly via modulating cell adhesion and suppressing TGF-β signaling pathway. - Source: PubMed
Publication date: 2026/07/06
Yu JiahaoWang XiaoyiJia LiyanFu LuluHe JunweiZhang ShanshanHe QiuxiaLiu KechunLi XiaobinLi Na - Intellectual disability (ID) affects approximately 1%-3% of the population and spans diverse clinical presentations with marked genetic heterogeneity, especially in consanguineous populations where autosomal-recessive ID is common. Despite advances in diagnostic methods, ~50% of individuals with ID remain without a molecular diagnosis. Genome sequencing (GS) can detect variant classes poorly captured by other methodologies, including deep intronic splice changes and structural variants. We performed short-read GS on 38 Iranian autosomal recessive intellectual disability (ARID) families that remained unsolved after exome sequencing (ES) and two phases of reanalysis. Sequencing and variant calling were performed on DRAGEN Bio-IT Platform with GRCh38 and variants were annotated in Golden helix Varseq software and the AnnotSV tool. GS yielded diagnoses in 2 of 38 families (5.3%), identifying a homozygous deep-intronic variant (c.1473 + 519C > T) that creates a cryptic donor site and a 57-bp pseudoexon, and a homozygous ~103-kb deletion removing the in-frame Exon 2. Additionally, GS uncovered a homozygous missense variant that represents a novel candidate gene for ARID, but further studies are required to confirm the gene-disease association. The and variants were uniquely detectable by GS. In conclusion, in a challenging, ES-negative ARID cohort, GS provided an additional ~5.3% diagnostic yield by uncovering a noncoding splice alteration and a large intragenic deletion. These results underscore GS as a valuable, though still modest, tool over ES and highlight significant interpretation challenges in noncoding regions. Continued advances in functional assays and complementary long-read technologies will be essential to further reduce the diagnostic gap in unresolved ID. - Source: PubMed
Publication date: 2026/07/01
Shokouhian EbrahimMoslemi MasoumehMoghadam Masoumeh GoleyjaniMolaei NegarAlagha ParnianReshadmanesh AzadehArzhangi SanazGhodratpour FatemehCelik MertKadioglu Ilayda SelcenEdizadeh MasoudAkbari Mohammad RezaKahrizi KimiaNajmabadi Hossein - 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