Ask about this productRelated genes to: NR2F2 Blocking Peptide
- Gene:
- NR2F2 NIH gene
- Name:
- nuclear receptor subfamily 2 group F member 2
- Previous symbol:
- ARP1, TFCOUP2
- Synonyms:
- COUP-TFII, COUPTFB, SVP40, NF-E3, COUPTF2
- Chromosome:
- 15q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-21
- Date modifiied:
- 2018-02-14
Related products to: NR2F2 Blocking Peptide
Related articles to: NR2F2 Blocking Peptide
- The human heart remains a central focus of biomedical research, yet capturing early chamber morphogenesis in vitro with structural and functional fidelity remains challenging. Here we show the generation of chamber-like cardiac organoids (CCOs) from human pluripotent stem cells that reproduce key features of heart chamber development. CCO formation is orchestrated by coordinated FGF, WNT, BMP, RA, and AA signaling, and regulated by transcription factors including HAND1, TFAP2B and NR2F2. These CCOs exhibit stable self-organized architectures with myocardial, endothelial layers and inner chamber, displaying spontaneous contraction and calcium transients. Single-cell transcriptomics revealed endothelium-to-cardiomyocyte interactions mediated by WNT2B, suggesting coordinated tissue patterning. We further validated the essential roles of RA and AA in modulating chamber enlargement and stability. Furthermore, CCOs enable efficient evaluation of cardiotoxicity and teratogenicity through direct visualization of drug-induced changes. Together, this platform provides a robust model for studying cardiac development, mechanistic research, and pharmacological screening. - Source: PubMed
Publication date: 2026/06/02
Zou XinleWang FanwenZheng HuilinLiu XianzhuangKong TianciJiang RuiGuo YingyingLiang YuZhao HanqingWang BoPei Duanqing - Atherosclerosis drives cardiovascular morbidity in diabetes, with endothelial-to-mesenchymal transition (EndMT) as a key contributor. Whereas epigenetic regulators are increasingly implicated in atherosclerotic progression, the specific role of enhancer of zeste homolog 2 (EZH2), a histone methyltransferase, in EndMT in diabetes-associated atherosclerosis remains unclear. We show that EZH2-mediated H3K27 (histone H3 at lysine-27) trimethylation is elevated in carotid plaques from patients with diabetes and in the aortic endothelium of diabetic mice. Pharmacologic EZH2 inhibition with GSK-126 attenuated EndMT and reduced atherosclerotic burden in diabetic mice. In human aortic endothelial cells exposed to high glucose/tumor necrosis factor-α or serum from patients with coronary artery disease, EZH2 blockade via GSK-126 or short hairpin RNA suppressed EndMT and reversed transcriptional programs assessed by RNA sequencing, including and . These findings identify EZH2 as a driver of EndMT in diabetes-associated atherosclerosis and highlight EZH2 inhibition as a potential therapeutic strategy to limit vascular pathology. - Source: PubMed
Publication date: 2026/05/29
Aziz MisbahSourris Karly CPinzon-Cortes Jairo ABlock Tomasz JDai AozhiMaxwell ScottOkabe JunCalkin Anna CCooper Mark EJandeleit-Dahm Karin A MKhan Abdul Waheed - Glioblastoma (GBM), a malignant brain tumor, is characterized by a high recurrence rate and poor overall survival. Therefore, understanding the causes of recurrence and identifying strategies for its prevention are crucial. To identify the characteristics of recurrent tumor samples and the molecular mechanisms of tumor progression, we conducted a longitudinal analysis of GBM using single-cell transcriptomics and clinical data from the Chinese Glioma Genome Atlas (CGGA). Compared to the primary tumor, recurrent GBM samples showed a more immunosuppressive environment. We identified an endothelial cell subpopulation, Edo4, that is characterized by high endothelial-to-mesenchymal transition (EMT) and is correlated with poor prognosis in recurrent tumors. It was regulated by the NR2F2 transcription factor specifically in the recurrent GBM samples. Cell-cell interaction analysis revealed that pericytes affect endothelial cell migration through the JAM2-(ITGA3+ITGB1) ligand-receptor axis, promoting GBM progression. Targeting the Edo4 cell cluster and the JAM2-(ITGA3+ITGB1) ligand-receptor pair may be a promising strategy to prevent GBM recurrence. - Source: PubMed
Publication date: 2026/04/22
He JingWang XunZhang SumeiGuo DanSun Jian - Osimertinib resistance represents a major therapeutic challenge in non-small cell lung cancer (NSCLC), yet the underlying epigenetic mechanisms remain incompletely understood. Through integrated epigenomic and transcriptomic profiling, we identified a resistance-specific, non-canonical transcriptional circuit driven by the coordinated action of three core components: ID3, SMAD3, and NR2F2. These transcription factors form protein complexes that co-bind to shared enhancers or promoters, reciprocally enhancing each other's transcriptional activity and that of their downstream targets. Mechanistically, ID3 mediates the chromatin residence of the SMAD3-NR2F2 complex through its non-canonical function as a structural co-factor. This rewires the transcriptional program of resistant cells to ultimately drive resistance via direct upregulation of HIF2A, a dual-function hub that concurrently promotes neuroendocrine differentiation and suppresses ferroptosis. Functional studies confirmed that disrupting this circuit or inhibiting its downstream effector HIF2A restored Osimertinib sensitivity in resistant models. Our study elucidates a novel epigenetic paradigm through which a non-canonical, self-reinforcing transcriptional circuit co-opts lineage plasticity and cell death evasion to drive Osimertinib resistance, thereby establishing a therapeutically actionable target for overcoming this aggressive phenotype. - Source: PubMed
Publication date: 2026/05/20
Liu AochuLiu ZhenguoJiang LizhenHuang AndongLin XinqingLi XinyueLiu BingyuanHu ShiwenPan QiangHuang JunjunYin LiyuanJiang LilingYi WeiMao WenjunZheng YueyuanShi Xianping - The ovary contains two major somatic lineages, granulosa cells and interstitial cells, that arise from progenitors within the coelomic epithelium. However, how these two lineages diverge during ovarian development remains unclear. By analyzing joint single-nucleus transcriptomic and chromatin accessibility profiles of murine ovarian cells at the onset of ovary formation, we identified two somatic progenitor populations from the coelomic epithelium distinguished by expression of the nuclear receptors and . Based on their transcriptomic trajectories, the epithelial cells preferentially transitioned toward the granulosa lineage whereas the epithelial cells differentiated into mesenchymal populations. This lineage relationship was supported by lineage tracing experiments that fetal progenitors contribute to ovarian interstitial cells postnatally. To define the molecular features underlying this divergence, we performed differential gene expression and chromatin accessibility analyses and found that epithelial cells, but not cells, were enriched for Notch pathway components and Notch effector motifs. Consistently, lineage tracing of Notch-responsive cells marked interstitial cells in postnatal ovaries, whereas ectopic Notch activation in cells promoted expansion of the interstitial population accompanied by reduced granulosa cells. By integrating motif analysis with accessible chromatin-gene linkage, we also identified downstream targets regulated by Notch effectors in cells, which showed concordant changes upon ectopic Notch activation. These findings demonstrate that somatic cell fate is established early during ovarian development, with active Notch signaling specifying the interstitial lineage and a balanced Notch activity required for proper somatic lineage establishment. - Source: PubMed
Publication date: 2026/04/22
Chen Yu-YingRattan SaniyaLiu ChangXu XinYao Humphrey H-C