Ask about this productRelated genes to: NR2C1 antibody
- Gene:
- NR2C1 NIH gene
- Name:
- nuclear receptor subfamily 2 group C member 1
- Previous symbol:
- TR2
- Synonyms:
- TR2-11
- Chromosome:
- 12q22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2016-11-09
Related products to: NR2C1 antibody
Related articles to: NR2C1 antibody
- Gastric cancer is a leading cause of cancer-related death, particularly in East Asia, yet its genetic basis remains incompletely understood. Using genome-wide association study data from BioBank Japan, we show that gastric cancer shares significant genetic associations with 25 other phenotypes, most notably cardiovascular conditions such as angina pectoris and myocardial infarction. Mendelian randomization supports a causal role of these traits in gastric cancer risk. Multitrait analysis of GWAS reveals a novel pleiotropic locus at 12q22 (rs12814712) that is shared between gastric cancer and cardiovascular traits. Functional experiments demonstrate that the risk allele at this locus reduces transcriptional activity and downregulates the expression of nearby genes, particularly VEZT. In gastric cancer cells, overexpression of VEZT and NR2C1 suppress proliferation and migration, whereas their knockdown promotes malignancy. Our analysis identifies rs12814712 as a novel susceptibility locus for gastric cancer and underscores its regulatory role in disease-related gene networks. - Source: PubMed
Publication date: 2026/03/15
Ding HuanxinLiu ChuxuanSun QingJiang YueXu QianZhu ZhenguoJin XinHuang QiboLi YueSong YingchaoLiu ZenglinYu TianmingShi BowenTan DelinLi LinzehaoMentch FrankGlessner JosephChang XiaoHakonarson HakonZhang Guangyong - Skeletal muscle development, a precisely orchestrated process, is vital for animal movement, energy metabolism, and meat production. Among Chinese poultry breeds, the Pekin duck and Liancheng duck are prominent, distinguished by their unique meat qualities and growth rates. In this study, we identified developmentally dynamic genes (DDG) by RNA sequencing of skeletal muscle tissues at different time points, from 1 to 42 days after birth, and found DDGs with opposite expression patterns in the early and late periods of skeletal muscle development. The high-to-low (earlyDDGs) and low-to-high (lateDDGs) expressed genes in two duck breeds, which show different functional enrichment features, were potentially regulated by different mutually inhibitory toggle-switch developmentally dynamic transcription factor (DDTF) pairs and alternative splicing. In Pekin ducks, interactions between earlyDDTFs (ZEB1, RORA, E2F6, PLAG1, MSANTD3) and lateDDTFs (ATF4, SIX2, ZBED4) predominantly affect earlyDDGs, prioritizing neuron establishment and optimization and lateDDGs enriched in VEGF-VEGFR2 signaling and cell division. In contrast, in Liancheng ducks, interactions between earlyDDTFs ATF2, FOXP2, NR2C1, GLIS2 and lateDDTFs ESRRB, MYCN are likely to affect earlyDDGs more involved in intracellular coordination and proliferation and lateDDGs involved in aerobic respiration and fatty acid beta-oxidation. Besides, differences in alternative splicing were observed for DDGs such as COL13A1 and RNF10, which may affect neurotransmission and vascular smooth muscle cell proliferation during skeletal muscle development between two duck breeds. These findings enhance our understanding of differences in regulatory mechanisms of skeletal muscle development between Pekin duck and Liancheng duck. - Source: PubMed
Publication date: 2025/08/15
Ding DingbangKinkpe LionelLi YangZhang YunshengWang Xia - The RNA helicase DDX41 is a DEAD-box helicase that is well known as a virus sensor in dendritic cells and a tumor suppressor that is frequently mutated in myeloid neoplasms. However, the functions and relevance of DDX41 in solid tumors remain largely unexplored. In this study, through in vivo CRISPR screening, we demonstrate that DDX41 is highly expressed in various solid tumor types and promotes tumorigenicity in liver cancer. Mechanistically, DDX41 facilitates R-loop processing and accelerates the transcription of RPL/RPS genes, thereby promoting ribosome biogenesis and protein synthesis. Additionally, we show that the acetyltransferase KAT8 is required for H3K9ac modification of the DDX41 promoter and that NR2C1/NR2C2 are responsible for DDX41 expression. Moreover, elevated DDX41 levels increase liver cancer cell sensitivity to protein synthesis inhibitors; treatment with homoharringtonine (HHT), an approved drug, significantly inhibits tumor growth in DDX41-overexpressing liver cancer models. Taken together, the results of this study highlight that DDX41 acts as an oncogene in liver cancer and suggest that protein synthesis inhibition may be a promising therapy for liver cancers with high DDX41 expression. - Source: PubMed
Publication date: 2025/08/11
Li HongquanHe YifeiJiang JiawenLiu ZhenLiu YizheShi QiliDing JieLi HaochenSun WeiliHu XinChen ZhiaoHe Xianghuo - Nuclear receptors regulate transcription in response to ligand signals and enable the pharmacological control of gene expression. However, many nuclear receptors are still poorly explored and are not accessible to ligand-based target identification studies. In particular, most members of the NR2 family are among the least studied proteins of the class, and apart from the retinoid X receptors (RXR), validated NR2 ligands are very rare. Here, we gathered the NR2 modulators reported in literature for comparative profiling in uniform test systems. Most candidate compounds displayed insufficient on-target activity or selectivity to be used as chemical tools for NR2 receptors underscoring the urgent need for further NR2 ligand development. Nevertheless, a small NR2 modulator set could be assembled for application in a chemogenomic fashion. There are 48 ligand-activated transcription factors in humans forming the superfamily of nuclear receptors (NRs, Figure 1a), which translate (endogenous) ligand signals into changes in gene expression patterns. The multifaceted roles of NRs span pivotal physiological processes, encompassing metabolism, inflammation, and cellular differentiation. Over decades, the NR1 and NR3 receptor families, including (steroid) hormone receptors and lipid sensors, have emerged as well-explored therapeutic targets of essential drugs like, for example, glucocorticoids as anti-inflammatory drugs, estrogen receptor modulators as contraceptives and anticancer agents, and PPAR agonists as oral antidiabetics. Despite this progress, a significant portion of the NR superfamily remains understudied, particularly within the NR2 family which comprises the hepatocyte nuclear factor-4 receptors (HNF4α/γ; NR2A1/2), the retinoid X receptors (RXRα/β/γ; NR2B1-3), the testicular receptors (TR2/4; NR2C1/2), the tailless-like receptors (TLX and PNR; NR2E1/3), and the COUP-TF-like receptors (COUP-TF1/2, V-erBA-related gene; NR2F1/2/6). Apart from RXR, all NR2 receptors are considered as orphan, and their ligands remain widely elusive. Therefore, chemical tools for most NR2 receptors are rare and poorly annotated posing an obstacle to target identification and validation studies. To enable chemogenomics on NR2 receptors and improve annotation, of the few available ligands, we gathered a scarce collection of NR2 modulators (agonists, antagonists, inverse agonists) for comparative evaluation and profiling. While the NR2B family (RXR) is well covered with high-quality ligands and a few early tools are available for NR2E1, we found the available ligands of the NR2A and NR2C families of insufficient quality to be used as chemical tools. - Source: PubMed
Publication date: 2025/02/20
Lewandowski MaxBusch RomyMarschner Julian AMerk Daniel - Recent empirical investigations reinforce the understanding of a profound interconnection between metabolic functions and Obstructive Sleep Apnea-hypopnea Syndrome (OSAHS). This study identifies distinctive miRNA signatures in OSAHS with Metabolic Syndrome (Mets) patients from healthy subjects, that could serve as diagnostic biomarkers or describe differential molecular mechanisms with potential therapeutic implications. In this study, OSAHS with MetS patients showed significantly higher Apnea Hyponea Index(AHI), but lower oxygen desaturation index(ODI 4/h) and minimum pulse oxygen saturation(SpO). A total of 33 differentially expressed miRNAs by Limma method, and 31 differentially expressed miRNAs by DEseq2 method were screened. In addition, GO enrichment analysis of target genes associated with differentially expressed miRNAs revealed significant enrichment in metabolic processes, suggesting that the differential expression of OSAHS-induced miRNAs may contribute to the progression of metabolic disorders through the regulation of metabolic pathways. Furthermore, KEGG pathway enrichment analysis revealed significant enrichment in the p53 signaling pathway and several other pathways. Notably, the Wnt signaling pathway, PI3K-Akt signaling pathway, cAMP signaling pathway, and AMPK signaling pathway are implicated in the metabolic processes of glucose dysregulation and lipid homeostasis, as well as the pathogenesis of hypertension associated with OSAHS. We identified IKBKB, PIK3R1, and MAP2K1 as the target genes most associated with Mets pathogenesis in OSAHS, regulated by miR-503-5p, miR-497-5p, and miR-497-5p, respectively. Additionally, the target genes of differentially expressed miRNAs between Tibetan OSAHS patients with MetS and healthy individuals are regulated by transcription factors such as NR2C1, STAT3, STAT5a, HIF1a, ETV4, NANOG, RELA, SP1, E2F1, NFKB1, AR, and MYC. In conlusion, we found differentially expressed miRNAs in Tibetan OSAHS patients with Metabolic Syndrome for the first time. Enrichment analysis results suggest that differentially expressed miRNAs may involved in the development of OSAHS-related metabolic disorders by regulating metabolic pathways. We also revealed that IKBKB, PIK3R1, and MAP2K1 are mostly associated with metabolic disorder in OSAHS, and miR-503-5p and miR-497-5p may regulate the development of MetS associated with OSAHS by modulating IKBKB, PIK3R1, and MAP2K1. - Source: PubMed
Publication date: 2025/01/23
Shi Xue-FengHe XiangSun Ze-RuiDuo JieYang Hao