Elf1 EMSA Kit
- Known as:
- Elf1 EMSA Kit
- Catalog number:
- AY1184
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- Elf1 EMSA Kit
Related genes to: Elf1 EMSA Kit
- Gene:
- ELF1 NIH gene
- Name:
- E74 like ETS transcription factor 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 13q14.11
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-23
- Date modifiied:
- 2016-10-05
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- In this study, we systematically analyzed the dynamic changes in chromatin accessibility and the transcriptional responses in the spleen of largemouth bass () following infection with iridovirus (LMBV) using the assay for transposase-accessible chromatin with sequencing (ATAC-seq) and transcriptome sequencing (RNA-seq). Based on post-infection survival status, largemouth bass were classified into a resistant group (SR) and a susceptible group (SS). A total of 11,317 differentially accessible regions were identified between the two groups, among which the chromatin accessibility of core promoter regions was entirely increased in the SR group, suggesting that chromatin remodeling in these regions may directly participate in the transcriptional regulation of immune-related genes. Functional enrichment analysis revealed that genes associated with differentially accessible regions were significantly enriched in immune-related pathways such as autophagy, apoptosis, Toll-like receptor signaling, and NOD-like receptor signaling. Motif analysis further identified that transcription factors significantly enriched in the SR group included CTCF and heterodimers composed of multiple members of the ETS and FOX transcription factor families. Through integrative analysis, seven transcription factors (CTCF, Spi1, ETV2::FOXI1, FOXJ2::ELF1, FOXO1::ELK1, SPIC, and FOXO1::ELF1) were found to be significantly enriched in core promoter regions. To further screen for differentially expressed genes directly regulated by chromatin accessibility changes, an overlapping analysis was performed between 629 predicted target genes and 2656 differentially expressed genes (DEGs), resulting in the identification of 71 candidate genes. Among these, three immune-related genes (, , and ) belonging to the ETS and FOX families were identified. This study reveals the dynamic chromatin accessibility landscape of largemouth bass in response to LMBV infection and demonstrates that increased chromatin accessibility in core promoter regions is closely associated with the resistant phenotype. Heterodimers of ETS and FOX family transcription factors may participate in antiviral immune responses by regulating the expression of key immune genes such as , , and , providing potential epigenetic molecular markers for disease resistance breeding in fish. - Source: PubMed
Publication date: 2026/05/05
Sun HuiHua JixiangTao YifanLu SiqiWang WenDong YalunZhang LinbingHe JixiangHe JieQiang Jun - Cell fate transitions are driven by regulatory circuitry, yet RNA velocity models cellular dynamics without explicitly accounting for gene regulatory interactions, limiting mechanistic insight. Conversely, gene regulatory network (GRN) inference methods largely neglect the dynamic nature of biological systems. To overcome this conceptual disconnect, we present RegVelo, a bottom-up, actionable, and interpretable deep learning framework that jointly models splicing kinetics and gene regulatory interactions. Across diverse biological systems, RegVelo provides reliable predictive power for terminal states, gene interactions, and perturbation simulations. By applying RegVelo to zebrafish neural crest development using full-length Smart-seq3 and shared gene expression and chromatin accessibility measurements, we delineate regulatory programs underlying fate specification. Guided by in silico perturbations and validated by CRISPR-Cas9 knockout and single-cell Perturb-seq, we establish tfec as an early driver and elf1 as a regulator of pigment cell fate. RegVelo establishes a quantitative framework for bridging gene regulation and cell fate decisions. - Source: PubMed
Publication date: 2026/05/11
Wang WeixuHu ZhiyuanWeiler PhilippMayes SarahLange MariusFountain Daniel MHaug Julianna OWang JingyeXue ZhengyuanSauka-Spengler TatjanaTheis Fabian J - Traumatic brain injury (TBI) disproportionately affects the elderly, yet the underlying mechanisms remain unclear. Here, we demonstrate that aged TBI brains predominantly harbor pro-inflammatory NLRP3+ microglia, in stark contrast to the neuroprotective Lysozyme+ microglia prevalent in young TBI brains. This age-dependent microglial dichotomy correlates with elevated mortality and impaired recovery in aged TBI mice. By leveraging an integrative multi-omics approach combined with metabolomics and epigenome analysis, we identify a previously unrecognized link between enhanced glycolysis and pro-inflammatory chromatin landscape in NLRP3+ microglia. Further investigation identifies ELF1 as a key transcription factor driving NLRP3+ microglia formation. Importantly, ablation of ELF1 reverses age-associated microglial dysfunction and improves TBI outcomes. Finally, we discover that Imeglimin, a clinically approved antihyperglycemic agent capable of crossing the blood brain barrier, inhibits ELF1 and reverses microglial phenotype, reducing acute mortality rate and leading to improved functional recovery of aged TBI mice. Our work elucidates the mechanistic basis of age-dependent TBI outcomes, reveals the crosstalk between metabolic rewiring and epigenetic regulation in microglial aging, and identifies ELF1 as a promising therapeutic target for improving TBI outcome. - Source: PubMed
Publication date: 2026/04/02
Lu ZhichaoShuai YiWang ChenxingLiu ZonghengWang ZihengLiu QianqianJiang RuiZhu JueZhu YongqiLiao WeiquanZhu XingjiaZhao JingweiShi KaibinShi WeiGong Peipei - Type 2 diabetes-associated osteoporosis (T2DOP) is characterized by progressive bone loss under chronic hyperglycemic stress; however, the contribution of ferroptosis to osteoblast dysfunction remains poorly understood. This study aimed to elucidate the molecular mechanisms driving osteoblast ferroptosis and senescence in T2DOP and to identify potential epigenetic regulatory targets. A streptozotocin/high-fat diet (STZ/HFD)-induced diabetic osteoporosis mouse model was established and exhibited significantly reduced bone mass. Diabetic femora and primary osteoblasts displayed prominent ferroptotic features, including increased lipid peroxidation and decreased GPX4 expression. Genetic deletion of Ifitm3 markedly alleviated ferroptosis and reduced cellular senescence (90% decrease in p21 expression). To examine the role of Ifitm3 in DOP, Ifitm3/ and Elf1/ mice were generated for functional assessment, and primary osteoblasts were isolated for in vitro experiments. A comprehensive approach was employed to elucidate the epigenetic and transcriptional regulation of Ifitm3 in DOP, integrating RNA sequencing (RNA-seq), m6A-MeRIP-seq, and MeRIP-qPCR. Additionally, we employed a variety of techniques, including μCT imaging, immunohistochemistry, immunofluorescence, ChIP-qPCR, dual-luciferase reporter assays, western blotting, and RNA pull-down experiments. Mechanistically, hyperglycemia activated the ETS transcription factor ELF1, which transcriptionally upregulated Igf2bp2, an N6-methyladenosine (m6A) reader protein. Mettl14-mediated m6A modification enhanced Ifitm3 mRNA stability through Igf2bp2 binding, as confirmed by MeRIP-qPCR and RNA decay assays. This Elf1-Igf2bp2-m6A-Ifitm3 cascade amplified lipid peroxidation and mitochondrial dysfunction in osteoblasts. Under the diabetic stress of the DOP model, this signaling axis exacerbated ferroptotic cell death, highlighting the pivotal role of Ifitm3 in mediating osteoblast dysfunction in DOP. Our study uncovers a previously unrecognized epigenetic ferroptosis pathway-the Elf1-Igf2bp2-m6A-Ifitm3-that critically contributes to osteoblast dysfunction in DOP, offering potential therapeutic targets for mitigating ferroptosis-related bone loss in diabetes. Targeting this signaling axis may offer a novel therapeutic strategy for diabetic osteoporosis. - Source: PubMed
Publication date: 2026/02/13
Liu Xiao-WeiZhang Shu-BaoXu Hao-WeiLu Jia-HaoChang Sheng-JieHuang Shan-ShanWang Shan-Jin - Mutation hotspots in melanoma frequently occur at DNA binding sites of ETS-family transcription factors, as ETS factors stimulate the formation of UV-induced cyclobutane pyrimidine dimers (CPDs) while suppressing repair at ETS-bound DNA sites. To elucidate the molecular mechanism by which ETS factors bind to damaged DNA sites and inhibit repair, we investigated the binding of members from the three major classes of the ETS superfamily (Ets1, ELF1 and PU.1) to cognate DNA containing a TpT CPD. These site-specific CPDs modulated ETS recognition and repair by a model repair enzyme in a position-dependent manner, with a deaminated CPD located in a damage hotspot in the ETS binding motif consistently stimulating binding and repair inhibition by all three paralogs. Co-crystal structures of PU.1 reveal that CPDs and mismatches are recognized within the framework of canonical ETS/DNA complexes, but with highly differentiated thermodynamic and dynamic properties. Specifically, the CPD-bound complex exhibits unique dynamics that reveal a novel DNA-binding mode as well as inform how ETS domains navigate the DNA conformational landscape to predispose CPD induction. The results offer a molecular rationale for how ETS factors induce mutation hotspots in skin cancers and other UV-exposed tissues by promoting CPD induction and inhibiting repair. - Source: PubMed
Publication date: 2026/01/14
Sivapragasam SmithaRoss Terrell JGermann Markus WLaughery Marian FEverly Michaela EAdhikari Shiva PHrdlicka Patrick JWyrick John JPoon Gregory M K