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
- : Uterine dysfunction contributes to infertility in PCOS. Jiawei Qi Gong Wan (JQGW) is used to improve endometrial homeostasis, but its mechanism is unclear. This study investigated whether JQGW improves uterine function via gut microbiota and metabolites. : Letrozole-induced PCOS mice received JQGW (low/high dose), metformin, or vehicle for 35 days. Endometrial morphology, receptivity genes, Akt2/NF-κB signaling, gut microbiota (16S rRNA), and serum metabolites (LC-MS) were assessed. : PCOS mice showed reduced endometrial thickness (126.4 ± 10.8 μm vs. 215.6 ± 12.3 μm in controls, < 0.001) and fewer glands (12.6 ± 1.8 vs. 28.4 ± 2.1, < 0.001). JQGW-H increased endometrial thickness (189.3 ± 11.2 μm, < 0.01 vs. PCOS) and gland number (23.1 ± 1.9, < 0.01 vs. PCOS), restored the receptivity markers (, , , and ) toward normal levels, suppressed Akt2/NF-κB activation, and reduced inflammatory cytokines. JQGW shifted the β-diversity structure of the gut microbiota toward the control pattern, with enrichment (LDA > 4). Four metabolites (PA(20:0/16:1(9Z)), 7-methylguanosine, methoxyacetic acid, 8.11-eicosadiynoic acid) showed nominal elevation in PCOS and negative correlations with endometrial thickness (r = -0.73 to -0.89, unadjusted < 0.01), although none survived FDR correction. : JQGW ameliorates PCOS-associated uterine dysfunction, potentially via gut microbiota and metabolite modulation. Future studies should validate causality using fertility-based outcomes and microbiota transplantation. - Source: PubMed
Publication date: 2026/07/24
Zheng RuqunSong JinlongLi JieShen YingyanLiu QiqiShi MengjiaZhuo YuxuanLuo HaoyuLi JingMa HongxiaHu MinWang Chi ChiuLi Juan - Therapeutic relapse driven by bortezomib resistance represents a formidable clinical barrier in the management of multiple myeloma (MM). Here, a carrier-free, supramolecular nanoplatform was engineered through the spontaneous co-assembly of two natural alkaloids, berberine (BBR) and nitidine chloride (NC), termed BBR/NC-SAPs, to counter this malignancy. Driven by cooperative π-π stacking and van der Waals forces, BBR/NC-SAPs display superior anti-MM efficacy and optimized biosafety as compared to the free-drug combination. Quantitative proteomics and functional landscapes showed that BBR/NC-SAPs robustly activate iron-dependent ferroptosis, as evidenced by massive lipid peroxidation, intracellular Fe overload, and mitochondrial depolarization. Mechanistically, integrated target deconvolution and atomistic molecular modeling identified NR2F2 as a direct target of BBR/NC-SAPs. Functional knock-out and rescue evaluations definitively validated that NR2F2 is an essential mediator governing the therapeutic response, as NR2F2 depletion occluded the ferroptotic cascade, and lentiviral reconstitution fully restored cellular sensitivity and GPX4-associated ferroptosis activation. Further, BBR/NC-SAPs markedly suppressed tumor growth and prolonged survival in bortezomib-resistant MM xenograft models, a therapeutic benefit actively reversed by the ferroptosis inhibitor ferrostatin-1. Collectively, this work highlights a paradigm of natural product-derived nanotechnology that targets the NR2F2-GPX4 axis, offering a promising supramolecular strategy to overcome drug resistance in refractory hematological tumors. - Source: PubMed
Publication date: 2026/08/18
Lv YiwenLiu ShuangWu HongLi GuiluanRong YingLi GuangchaoZhu YangminZhong QiOu RuimingShen HuijuanLiu ZhiHuang JingWang ZhenweiLin PeiZhang QingYu GuopanYin Zhao - Although FMS-like tyrosine kinase-3 (FLT3) inhibitors initially induce a favorable response in AML patients, their long-term efficacy is often limited by the development of resistance. Bone marrow stromal cells (BMSCs), a key component of AML bone marrow niche, support leukemia cell survival and drive drug resistance through multiple approaches like direct contact, cytokine secretion, and exosome release. BMSC-mediated AML resistance involves complex and heterogeneous mechanisms that vary depending on the drug type and the characteristics of the leukemic cells. Therefore, this study seeks to elucidate how BMSCs interact with FLT3-ITD-mutated AML cells to confer FLT3 inhibitor resistance, aiming to identifying potential therapeutic targets to overcome such resistance. We discovered that BMSCs co-cultured with leukemia cells exhibited elevated expression of COX-2 and its product PGE2. BMSC-derived PGE2 suppressed ferroptosis in AML cells by modulating fatty acid metabolism and enhancing the glutathione antioxidant system. Additionally, PGE2 activated the GSK3β/β-catenin signaling pathway, facilitating the nuclear translocation of β-catenin, which influenced the apoptotic rates of AML cells. Proinflammatory cytokines such as TNF-α and IL-1β secreted by FLT3-ITD-mutated AML cells suppressed NR2F2 expression in BMSCs, leading to de-repression of COX-2 and subsequent PGE2 secretion, further amplifying this regulatory loop. Taken together, our findings reveal a novel mechanism whereby the NR2F2/COX-2/PGE2 axis modulates the sensitivity of AML cells to FLT3 inhibitors, and targeting this circuit may serve as an adjuvant therapy to improve FLT3 inhibitor efficacy. - Source: PubMed
Publication date: 2026/08/11
Wang JingmingTang LuJiang HuiwenYin HaifengLi YingyingChen ZhaozhaoXie QinyingWu ZhongZhang WanyingShu JinhuiWang MoranMei HengHu Yu - Blood-brain barrier (BBB) integrity naturally declines with age. Brain endothelial cells (ECs) and pericytes (PCs) form the BBB, and aging impairs tight junctions, likely via altered PC-to-EC signaling. However, the molecular mechanisms underlying this impairment remain unclear. Using single-cell RNA sequencing, we profiled 68,316 brain ECs expressing 15,564 genes from young and old mice. Unsupervised clustering and annotation revealed five distinct EC subtypes-Capillary EC1, Capillary EC2, Arterial EC, Venous EC1, and Venous EC2-defined by marker genes , and , respectively. Aging shifted EC subtype distribution, with reduced Capillary EC1 (45% vs. 57%) and increased Arterial (33% vs. 16%) and Venous ECs (12% vs. 2%) compared with young mice. Mio analysis further showed that Capillary EC1 and Venous EC2 neighborhoods were less abundant in aged brains. Biotin metabolism was decreased in old vs. young mice, particularly within Capillary EC1, Capillary EC2, and Arterial EC. Although widespread gene downregulation was observed across EC subsets, overall expression trends were largely consistent among clusters. Key genes--were less abundant, whereas was uniquely enriched in aged mice. Immunohistochemistry confirmed reduced LY6C and RAMP2 and elevated RASGRF2 in aged mouse and human brains. Cell-cell interaction analyses revealed age-associated remodeling of ligand-receptor signaling. Enrichment analyses implicated pathways involved in neurovascular integrity, inflammation, amyloid processing, and vascular remodeling. Collectively, these findings show that aging reprograms EC subtype composition, gene expression, and metabolism, thereby contributing to BBB disruption and neurovascular dysfunction. - Source: PubMed
Publication date: 2026/07/31
Nguyen Hai DucSiddiqui SummerBohannon Diana GBlair Robert VDeng Hong-WenPrat AlexandreKim Woong-Ki - In vitro maturation (IVM) of germinal vesicle oocytes may broaden assisted reproductive technologies; however, developmental competence remains limited by the lack of standardized follicular somatic support. We generated an endogenous FOXL2-P2A-tdTomato reporter human induced pluripotent stem cell (hiPSC) line using CRISPR/Cas9 knock-in and reporter-guided transcription factor (TF) programming to produce fetal granulosa-like cells (FGLCs). A flow cytometric TF screen identified TCF21, WT1-KTS, and NR1H4 as the strongest FOXL2 inducers, and combinatorial optimization showed that removing TOX3/ETV5 and adding NR2F2 substantially increased the FOXL2-positive fraction. Bulk RNA-seq, principal component analysis, and TF activity inference positioned the induced cells close to early-gestational human fetal granulosa cell profiles. In a mouse IVM, in vitro fertilization (IVF), blastocyst culture, and embryo transfer pipeline, FGLC supplementation did not change nuclear maturation rates but improved downstream development, most clearly increasing offspring production from cumulus-oocyte complexes. A comprehensive safety assessment of F0 offspring derived from FGLC-treated oocytes revealed a normal sex ratio, postnatal growth, gross anatomy, gonadal histology, and modified SHIRPA neurobehavioral profiles. Next-generation natural mating and germ cell assays demonstrated preserved fertility, normal IVF outcomes, and normal sperm parameters in the F1 generation. These results establish a scalable strategy for generating fetal granulosa-like supporting cells from hiPSCs and provide an effective and multi-generational safety framework for oocyte-contact IVM interventions. - Source: PubMed
Publication date: 2026/07/24
Imura-Kishi KasaneYamaga KatsumaSoeda ShouMasuda KeisukeMizoue YukiKoga ReiriTorigoe DaisukeMiyazaki HirokiSato IoriHikabe OrieKojima KazuakiTakeo ToruHamazaki NobuhikoSeita Yasunari