Ask about this productRelated genes to: E2F2 antibody
- Gene:
- E2F2 NIH gene
- Name:
- E2F transcription factor 2
- Previous symbol:
- -
- Synonyms:
- E2F-2
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-31
- Date modifiied:
- 2016-10-05
Related products to: E2F2 antibody
Related articles to: E2F2 antibody
- Fetal skeletal muscle development involves coordinated interactions among myogenic, stromal, vascular, and immune compartments, yet the cellular and molecular programs guiding tissue maturation remain incompletely understood. To address this, we generated a high-resolution single-cell atlas of fetal female goat skeletal muscle and performed trajectory analysis, transcription factor activity profiling, and intercellular communication mapping. Unsupervised clustering identified RUNX2 mesenchymal progenitors, fibro-adipogenic progenitors (FAPs), myofibroblasts, endothelial cells, macrophages, differentiating myocytes, and mature skeletal muscle fibers, revealing a heterogeneous ecosystem in which stromal populations support myogenic progression and vascular and immune cells contribute to tissue organization. Pseudotime analysis traced a maturation continuum from differentiation-competent myocytes to contractile fibers, marked by sequential activation of extracellular matrix remodeling, cytoskeletal stabilization, and sarcomere assembly. KEGG and GO enrichment highlighted stage-specific engagement of ErbB, Hedgehog, and Hippo signaling, as well as cell cycle and ubiquitin-mediated proteolysis pathways, linking proliferation, differentiation, and structural maturation. Transcription factor profiling revealed early-stage proliferative and morphogenetically permissive states driven by E2F4/5, HMGA2, and HAND2, transitioning to late-stage differentiation, ECM remodeling, and tissue stabilization orchestrated by CEBPB, CREB3L1, ELK1, and E2F2. Cell-cell communication analysis showed a developmental redistribution of signaling authority, from ECM-driven, progenitor-centered networks to modular, structurally stabilized interactions. These findings define the cellular, transcriptional, and signaling framework orchestrating fetal skeletal muscle maturation. - Source: PubMed
Publication date: 2026/04/29
Han ShiyaoXie ShengcanJiang FenfenZou QianhuiLi TianleWang AhuiWang NanLei ChuzhaoTang Young - Systemic lupus erythematosus (SLE) is a chronic autoimmune disease influenced by multiple genetic and environmental factors.. This study used bioinformatics to identify new diagnostic biomarkers and explore the pathogenesis of SLE. - Source: PubMed
Publication date: 2026/05/11
Pan QingboYu XuliangZhu JinZheng Xiaojin - IntroductionHead and neck squamous cell carcinoma (HNSCC) is characterized by metabolic reprogramming and poor prognosis. While lactate accumulates in HNSCC, how upstream RNA regulation coordinates lactate-associated epigenetic alterations during tumor progression remains unclear.MethodsWe integrated TCGA-HNSCC analyses, paired clinical specimens, and in vitro functional assays with mechanistic readouts including RIP-qPCR and LDHA 3'UTR luciferase reporters. Lactate was quantified in culture supernatants, H4K8la was assessed by immunoblotting and tissue IF, and H4K8la CUT&Tag was performed as an exploratory chromatin profiling assay.ResultsIGF2BP3 was upregulated in HNSCC and associated with adverse survival in public datasets. IGF2BP3 silencing inhibited proliferation, migration, and invasion. Mechanistically, IGF2BP3 bound LDHA mRNA and promoted LDHA expression via an mA-site-dependent LDHA 3'UTR mechanism, increasing lactate and H4K8la; exogenous lactate partially restored H4K8la under pH-matched conditions. Exploratory H4K8la CUT&Tag suggested increased H4K8la signal at the E2F2 locus with enrichment of cell-cycle programs upon lactate treatment.ConclusionThese findings support an IGF2BP3-LDHA-lactate-H4K8la axis linking post-transcriptional regulation to metabolic and chromatin remodeling in HNSCC. - Source: PubMed
Publication date: 2026/04/25
Wu FanZeng YuluHu YunlongXie ZihuiShen RongZhou JiaxinZhou PingtingTong ShanshanLiu Yehai - Renal cell carcinoma (RCC) ranks as the most prevalent form of urogenital cancer. This research aims to investigate the role of YTHDF2 in the RCC progression and identify new therapeutic targets for RCC. YTHDF2, E2F2, and CORO6 were assayed via qRT-PCR and Western blot. YTHDF2 was downregulated in RCC cells, while E2F2 and CORO6 were upregulated. After overexpressing YTHDF2 in RCC cells, cell viability, proliferation, invasion, and migration were measured. m6A levels were assessed. The binding of YTHDF2 to E2F2 was detected. The E2F2 mRNA stability was detected. The binding of E2F2 to the CORO6 promoter was analyzed. Overexpression of E2F2 or CORO6 was combined with YTHDF2 overexpression to validate the mechanism. Tumor growth and metastasis were observed. Results confirmed that YTHDF2 overexpression decreased cell proliferation, invasion, and migration. YTHDF2 bound to the m6A sites on E2F2 mRNA, promoted E2F2 degradation, and inhibited E2F2 expression. E2F2 bound to the CORO6 promoter to enhance CORO6 expression. Overexpression of E2F2 or CORO6 partially reversed the suppressive effects of YTHDF2 overexpression on RCC cell proliferation and invasion. YTHDF2 overexpression suppressed tumor growth and metastasis. In conclusion, YTHDF2 overexpression suppresses RCC progression by inhibiting E2F2 expression and reducing CORO6 expression via m6A modification. - Source: PubMed
Zhang XiaomengZhang YanYang XinFan YeZhu Yingying - Chronic heart failure (CHF) represents a major global health burden characterized by complex pathologies. The Yi Qi Huo Xue compound prescription (YQHXCP) has demonstrated significant clinical efficacy in alleviating heart failure symptoms; however, its precise molecular mechanisms remain obscure. - Source: PubMed
Publication date: 2026/03/23
Liao JiadanWang PengchengWu ZuoyueCui JuanShen PeiyunChen Xufeng