ETV4 _ E1A_F EMSA Probe Set
- Known as:
- ETV4 _ E1A_F EMSA Probe Set
- Catalog number:
- AY1308P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- ETV4 _ E1A_F EMSA Probe Set
Related genes to: ETV4 _ E1A_F EMSA Probe Set
- Gene:
- ETV4 NIH gene
- Name:
- ETS variant 4
- Previous symbol:
- -
- Synonyms:
- E1A-F, E1AF, PEA3
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-27
- Date modifiied:
- 2016-02-25
Related products to: ETV4 _ E1A_F EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: ETV4 _ E1A_F EMSA Probe Set
- Enamel is asymmetrically distributed in mouse incisors, which grow throughout life, and this continuous renewal is driven by dental epithelial stem cells (DESCs). In this study, we report that ablation of Isl1 in the dental epithelium using Pitx2-Cre leads to impaired development of the mandibular incisors. In Isl1 mutant embryos, the mandibular incisors exhibited a significant reduction in size and length compared to wild-type controls. A significant decrease in the proliferation of epithelial and mesenchymal cells was also detected in Isl1 mutant incisors, and cell apoptosis was markedly increased in the lateral cervical loop of Isl1 mutant incisors at E17.5. Ameloblasts and enamel were present on all surfaces of the mandibular incisor, including the labial side. Transcriptome analysis and in situ hybridisation revealed that Isl1 deletion induced significant upregulation of Hedgehog pathway components (Shh, Ptch1, Gli1) and FGF signalling mediators (Fgf3, Etv4, Etv5), while downregulating dental epithelial stem cell markers Sox2 and Lgr5. Our results showed that ISL1 co-localised with SOX2 in the lingual and lateral dental epithelium of mandibular incisors, and the expression of Sox2 was regulated by Isl1. Our results demonstrate that Isl1 sustains DESC viability and orchestrates ameloblast lineage commitment via SOX2-mediated regulation during incisor morphogenesis. - Source: PubMed
Publication date: 2026/08/27
Qu YapingLiu HuizhouWang YanGao ShanhuiHuang HuarongLi JianyingQiu MengshengLi Feixue - Stromal cell states are altered in active Crohn's disease (CD), but their origin and phenotypic stability are unknown. Using single-cell spatial transcriptomics, RNA sequencing and ATAC sequencing of ~2,500,000 cells, we map 18 distinct stromal cell states within their cellular and cytokine signaling environments in human full-thickness CD bowel. Inflammatory fibroblasts (IFs) reside in immune cell-rich mucosal ulcers and are induced through combinatorial cytokine exposure suppressing submucosal universal fibroblast programs. The IF state is stabilized through transcription factor (TF) activity of GLI3, TWIST1, ETV4, PRDM1 and RELB, and does not spontaneously revert; however, histone deacetylase inhibition destabilizes the IF state, preventing IF secretome-induced epithelial transmigration and activation of neutrophils. The IF open chromatin configuration is distinct from that of fibrotic contractile stroma, which populate adjoining immune-depleted submucosal fibrotic niches. These findings show that microenvironments in pathological tissue niches shape open chromatin configuration of stromal states that are amenable to modulation by epigenetic modifiers. - Source: PubMed
Publication date: 2026/08/12
Koplev SimonSharma OsheenWoelfel SimonHuang NiPohin MathildeFeile AdrianWarschinke MariaArtero Mikel RezolaSuthakaran SharujanSarropoulos IoannisPett J PatrickNyman JuliaThomas TomPham DuyLi BinAttar MoustafaPakpoor JuliaMilosevic-Hutton KateEaston AlistairButler MattDunford JamesPhilpott MartinColes MarkBuckley Christopher DDendrou CalliopeShamiyah KhalidKretschmer LorenzDratva LisaIssa FadiHester JoannaRittscher JensWalsh AlissaTravis Simon PProgatzky FränzeUnger Lukas WBignell MarkBaker KatherineGeorge BruceAl-Mossawi HusseinKlenerman PaulMosig Alexander SOppermann UdoTeichmann Sarah APowrie Fiona MFriedrich Matthias - ETV4 (ETS-transformation-specific variant 4) is a member of the ETS transcription factor family that has been extensively studied for its oncogenic functions in cancers. Here, we summarize the role and mechanisms of ETV4 in cancer biology, with a particular focus on colorectal cancer (CRC), as well as its biomarkers and therapeutic potential. As a transcription factor, ETV4 regulates the expression of target genes by recognizing the GGA(A/T) core conserved sequence. It is frequently overexpressed in pan-cancer, where its overexpression associated with poor prognosis. Upon activation by oncogenic signaling pathways (e.g., MAPK, PI3K/Akt, and WNT), ETV4 transcriptionally regulates downstream genes to promote tumor cell proliferation, invasion, migration, epithelial-mesenchymal transition (EMT), chemoresistance, metabolic reprogramming, and immune evasion. It also form a vicious positive feedback loop that continuously activates oncogenic signaling. In CRC, ETV4 is overexpressed, correlating with advanced disease, lymph node metastasis, and poor prognosis. Upon activation by oncogenic signals, ETV4 directly activate target genes (such as matrix metalloproteinases) to mediate adenoma-to-adenocarcinoma progression, proliferation, EMT, ferroptosis, invasion, metastasis, metabolic reprogramming, and tumor microenvironment remodeling in CRC. ETV4 also forms transcriptional complexes with certain epigenetic factors, such as miRNAs and p300. Moreover, ETV4 is a promising biomarker for CRC diagnosis, prognosis, and adenoma-to-adenocarcinoma progression. Targeting ETV4 or its upstream pathways represents a potential therapeutic strategy for CRC. However, there are still many unresolved issues in current research. For example, the role of ETV4 in immune evasion and tumor microenvironment remodeling remains at the descriptive stage, and the specific mechanisms by which it regulates immune cell recruitment have not yet been elucidated. Future efforts include utilizing multi-omics approaches to elucidate the mechanisms by which ETV4 shapes the CRC microenvironment and exploring the application prospects in tumor immunotherapy. - Source: PubMed
Publication date: 2026/07/15
Liu YuanbinWang YiyunHuang MinTian XiaHuang Xiaodong - Matrix metalloproteinase-9 (MMP9) is involved in extracellular matrix remodeling, inflammation, and metastasis, and its overexpression is associated with poor prognosis in lung cancer. However, the systems-level effects of MMP9 inhibition remain incompletely understood. We combined systems biology with experimental validation to characterize MMP9-centered signaling in non-small cell lung cancer (NSCLC) and identify downstream pharmacodynamic biomarkers. Network and pathway analyses revealed extracellular matrix- and inflammation-related interaction modules and prioritized an -associated gene panel. Synthesized compounds were evaluated using purified enzyme assays and A549 NSCLC cells. At 50 μM, compounds M34 and M33 showed the strongest inhibition of MMP9 activity (65.01% and 61.32%, respectively). Seven compounds (M1, M2, M8, M9, M10, M27, and M34) demonstrated antiproliferative activity at 72 h (IC = 40-115 μM), suppressed migration and colony formation, induced apoptosis, and reduced MMP9 protein expression. Quantitative PCR confirmed coordinated downregulation of , , , and , with upregulation of , , , , and . Enrichment analysis linked these changes to inflammatory signaling, immune activation, and extracellular matrix remodeling. These findings establish an experimentally supported eight-gene pharmacodynamic biomarker signature and support biomarker-guided development of MMP9-targeted strategies in NSCLC. - Source: PubMed
Publication date: 2026/07/20
Rashid Zainab AhmedHajjo RimaSabbah Dima ASweidan KamalAlmutairi ShriefaBardaweel Sanaa K - The E26 transformation-specific family of transcription factors regulates the cell cycle and apoptosis that are crucial for carcinogenesis. More specifically, the PEA3 subfamily-comprising ETS variant (ETV) transcription factors ETV1, ETV4, and ETV5-has been implicated in multiple oncogenic signaling pathways and chemotherapy resistance. While cisplatin is still a widely used chemotherapeutic treatment for ovarian cancer, its therapeutic efficacy is sometimes limited by the induction of resistance mechanisms. The present study investigates the potential role of PEA3 subfamily genes in cisplatin resistance in ovarian cancer through comprehensive in silico analyses. - Source: PubMed
Publication date: 2026/04/21
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