Recombinant EBOV VP40 protein
- Known as:
- Recombinant EBOV VP40 protein
- Catalog number:
- 0564-001
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- IBT Bioservices
- Gene target:
- Recombinant EBOV VP40 protein
Related genes to: Recombinant EBOV VP40 protein
- 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: Recombinant EBOV VP40 protein
Related articles to: Recombinant EBOV VP40 protein
- The high heterogeneity of lung adenocarcinoma (LUAD) is largely due to its complex tumor immune microenvironment (TIME). Cancer-associated fibroblasts (CAFs) are a core matrix component of TIME. However, their functional heterogeneity and the specific molecular mechanisms driving tumor progression have not been fully elucidated. In addition, the role of nuclear receptor NR2F2 in tumor development is still controversial. - Source: PubMed
Publication date: 2026/04/13
Zhou SongGuo YiboCheng RunjieZhang QianqianXing YuanxinGeng YizhenYang JinzeHan XiaoguangZhang YingXie Wei - Diffuse large B-cell lymphoma (DLBCL) represents the most prevalent form of non-Hodgkin lymphoma, distinguished by its aggressive clinical presentation and poor patient outcomes. This study investigated the role of nuclear receptor subfamily 2 group F member 2 (NR2F2) and 14-3-3 epsilon (YWHAE) in DLBCL progression. NR2F2 and YWHAE were highly expressed in DLBCL cell lines and tumor tissues of patients with DLBCL. Elevated expression of both genes correlated with advanced Ann Arbor stage and higher International Prognostic Index scores in DLBCL patients. Functional assays demonstrated that knockdown of NR2F2 or YWHAE suppressed DLBCL cell proliferation, migration, and invasion, as well as tumor growth in xenograft models. Mechanistically, NR2F2 transcriptionally activated YWHAE by binding to its promoter, thereby promoting phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling. Notably, treatment with a PI3K activator in YWHAE-silenced cells, or YWHAE overexpression in NR2F2-silenced cells, partially reversed the inhibitory effects on malignant behaviors of DLBCL cells. Collectively, these findings indicate that NR2F2 promotes DLBCL progression through transcriptional activation of YWHAE and subsequent activation of the PI3K/AKT pathway, suggesting a potential therapeutic target for DLBCL. - Source: PubMed
Publication date: 2026/04/22
Yu LiqianWang YingweiLi TiantianHe XiaoxueWang Wei - Hepatocellular carcinoma (HCC) is a metabolically active malignancy. Cuproptosis, a copper-dependent programmed cell death pathway, has been found to be closely associated with tumor progression. Cells with strong oxidative phosphorylation (OXPHOS) capacity exhibit heightened susceptibility to cuproptosis. We demonstrate that the tumor suppressor ASPP2 regulates the key cuproptosis modulator FDX1 by promoting NR2F2 recruitment to the FDX1 promoter in HCC. ASPP2 promotes intracellular copper accumulation through lipoylated protein oligomerization, thereby inducing cuproptosis. Furthermore, ASPP2 facilitates mitochondrial OXPHOS via enhanced tricarboxylic acid (TCA) cycle activity, which sensitizes HCC cells to cuproptosis. In vitro and in vivo experiments confirmed that ASPP2 overexpression suppresses tumor growth and synergizes with copper ionophores. Clinical specimen analysis revealed ASPP2-FDX1 co-expression in 90 HCC cases. A prognostic model incorporating ASPP2 and cuproptosis-related genes demonstrates superior survival prediction in TCGA cohorts. These findings establish the ASPP2-FDX1-NR2F2 axis as a metabolic-cuproptosis link and propose a novel therapeutic strategy for HCC. - Source: PubMed
Publication date: 2026/04/24
Yang LuLi XuhuiJiang YutongZhang MingzhuWu TiantianPi PeixianHan ZhuozhuoZhang ZhiyuKong FangyuanLu XiuhongYang HaoZuo ChaohuiHuang GangZhao JianLiang Beibei - Microvessels within atherosclerotic plaques are crucially involved in disease progression. Here, we generated a transcriptomic atlas of human atherosclerosis at single-cell resolution, encompassing 17,367 vascular endothelial cells (VECs) from five scRNA-seq studies, and verified key morphological characteristics using histology. SULF1 arterial endothelial cells (ArtECs) represented the primary subcluster undergoing endothelial-to-mesenchymal transition (EndMT). Capillary-like endothelial cells (CapECs) were identified as primary mediators of angiogenesis, and a trajectory model illustrated the transition between tip and stalk cells, with subclusters of ArtECs and CapECs predominantly expressing CXCL12, thereby driving the CXCL12/CXCR4 signaling axis. The largest plaque EC cluster, exhibiting the most heterogeneity, was found among post-capillary venule endothelial cells (VenECs), particularly ACKR1NR2F2 VenECs, which displayed distinct inflammatory transcriptional signatures characterized by adhesion molecules and chemokines. Overall, this atlas of atherosclerosis underscores endothelial heterogeneity and identifies SULF1 ArtECs and VenECs as potential therapeutic targets for EndMT and leukocyte recruitment, respectively. - Source: PubMed
Publication date: 2026/04/17
Wu YanzhaoXue ZhiweiSun TaoYu YindaLiang XiangjunXing WenchenMu FeiyuZhang ZhihanLv MeilinLing LuHan MengtaoCheng LianGisterå AntonWang Donghai - - Source: PubMed
Publication date: 2026/04/09
Liu JinlingLiu JiaoLi HaihuiKong LinlingHu YaqinZhou Lu