E2F2 antibody - middle region (ARP31611_P050)
- Known as:
- E2F2 (anti-) - middle region (ARP31611_P050)
- Catalog number:
- arp31611_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- E2F2 antibody - middle region (ARP31611_P050)
Related genes to: E2F2 antibody - middle region (ARP31611_P050)
- 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 - middle region (ARP31611_P050)
Related articles to: E2F2 antibody - middle region (ARP31611_P050)
- 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 - Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction. Growing evidence highlights the critical role of lncRNAs in RA initiation and progression. However, the pathogenic contributions of many lncRNAs remain unclear. - Source: PubMed
Publication date: 2026/03/18
Wang YuqunLiu JunhongDu LinpingWang XiaodongSu Yuhua - Oxaliplatin, a widely used chemotherapeutic agent, is associated with hematologic toxicities such as anemia, leukopenia, and thrombocytopenia. Despite their clinical relevance, the molecular mechanisms underlying lineage-specific bone marrow suppression remain poorly understood. - Source: PubMed
Publication date: 2026/02/16
Sudlow Leland CDu JunweiShahverdi KianaZhou HaiyingBerezin Mikhail Y - Cell senescence has been widely demonstrated to limit the osteogenic and odontogenic potential of human dental pulp stem cells (DPSCs). This study aimed to elucidate the regulatory mechanism by which E2F transcription factor 2 (E2F2) influences senescence and osteogenic differentiation in young DPSCs (yDPSCs). yDPSCs and old DPSCs (oDPSCs) were isolated and characterized by flow cytometry. The endogenous expression levels of E2F2, methyltransferase-like 3 (METTL3), and senescence- or osteogenesis-related markers were determined by qRT-PCR and Western blot. Senescence-associated β-galactosidase (SA-β-gal) staining was performed to assess cell senescence, while Alizarin Red S (ARS) and alkaline phosphatase (ALP) staining were used to evaluate the osteogenic differentiation capacity of yDPSCs. Dual-luciferase reporter and chromatin immunoprecipitation assays were conducted to confirm molecular interactions. Both yDPSCs and oDPSCs were positive for CD73 and CD105 and negative for HLA-DR. Compared with oDPSCs, yDPSCs exhibited stronger osteogenic differentiation potential and higher E2F2 expression. Knockdown of E2F2 increased the proportion of SA-β-gal-positive cells and upregulated the senescence markers p21 and p16, while it suppressed mineralization, ALP activity, and the expression of osteogenesis-associated markers (BMP2, OCN, OPN, Runx2, Osterix) in yDPSCs. Mechanistically, METTL3 was identified as a transcriptional target of E2F2. Overexpression of METTL3 reversed the inhibitory effects of E2F2 knockdown on odontogenic/osteogenic differentiation and the promoting effects on cell senescence in yDPSCs. E2F2 plays a critical role in suppressing DPSC senescence and promoting their osteogenic differentiation. - Source: PubMed
Publication date: 2026/03/20
Yang JiyongZhao SuliYang KunFeng DandanXiang JunZhang Yuanxiu - Human alpha-herpesvirus 1 (HSV-1) acute infection culminates in life-long latency in sensory neurons in trigeminal ganglia and certain neurons in the central nervous system. Previously, E2F family members and glucocorticoid receptor (GR) were shown to stimulate HSV-1 and bovine herpesvirus 1 (BoHV-1) replication. Consequently, we hypothesized GR and E2F family members activate certain HSV-l promoters. To test this hypothesis, we determined if four HSV-1 ICP0 cis-regulatory modules (CRM) upstream of the ICP0 promoter were activated by E2F. GR and E2F2, but not E2F1, E2F3a, or E2F3b, cooperatively transactivate the ICP0 CRM-C, but not CRM-A, -B, or -D fragments upstream of a minimal promoter in a luciferase reporter construct. CRM-C sequences contain two E2F consensus binding sites, a GC-rich motif that E2F2 can bind, and a consensus ½ GR response element (GRE) adjacent to the consensus E2F #2 binding site. Mutating the ½ GRE or the 3 E2F binding sites significantly reduced GR- and E2F2-mediated transactivation. Chromatin immunoprecipitation studies revealed E2F2 occupied ICP0 CRM-C sequences during productive infection and mutating the E2F binding sites prevented E2F2 binding. These studies reveal GR and E2F2 transactivate ICP0-promoter activity, which may enhance viral replication in certain cell types. - Source: PubMed
Publication date: 2026/03/02
Jayathilake KaushalyaSantos Vanessa ClaireJones Clinton