Ask about this productRelated genes to: E2F3 Blocking Peptide
- Gene:
- E2F3 NIH gene
- Name:
- E2F transcription factor 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-31
- Date modifiied:
- 2016-10-05
Related products to: E2F3 Blocking Peptide
Related articles to: E2F3 Blocking Peptide
- We aimed to investigate whether N6-methyladenosine (m⁶A) methylation modification mediated by METTL3 regulates the senescence of SCAPs, and to elucidate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/05/18
Sun ChengFang YuxinLi ZehanLi Wuli - Corymbia citriodora wood holds extensive application value; however, due to the cross-pollination nature of C. citriodora and the significant genetic variation among offspring, a phenomenon is observed in plantations where trees with the same parental lineage exhibit varying diameter at breast height (DBH). In this study, we hypothesized that the observed DBH variation reflects two divergent adaptation strategies under winter conditions: smaller trees may exhibit heightened cold sensitivity, activating stress responses and entering early dormancy, whereas larger trees may sustain cambial activity through coordinated regulation of cell-cycle genes and carbohydrate metabolism. - Source: PubMed
Publication date: 2026/05/06
Wang ChubiaoLiu XiangSu ZhikangHe WenliangOu Yuduan - Osteosarcoma (OS) is a malignant bone tumor originating directly from bone tissue, predominantly affecting adolescents. Cisplatin (DDP)-based chemotherapy is commonly used in the treatment of OS, but the emergence of DDP resistance poses a significant challenge to effective management. The study aimed to investigate the role of circRNA VANGL1 (circVANGL1) in mediating DDP resistance in OS in vitro. - Source: PubMed
Publication date: 2026/05/06
Mo FanWang HaoXie QiHuang DahongYang Yuan - Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest cancers with limited therapeutic options. Dysregulated transcriptional networks are key drivers of its aggressive biology. Here, by integrating clinical datasets with mechanistic studies, we performed a family wide systematic analysis of E2F transcription factors and identified E2F3 as a key oncogenic driver with prognostic significance comparable to E2F1. Functional studies showed that E2F3 accelerates PDAC proliferation and xenograft growth. Mechanistically, E2F3 transcriptionally activates the E3 ligase TRIM26, which binds TAB1, promotes K11-linked polyubiquitination, and facilitates TAB1-TAK1 complex formation to engage canonical NF-κB signaling. The SPRY and RING domains of TRIM26 mediate TAB1 interaction and ubiquitination, respectively. TRIM26 depletion attenuated E2F3 induced NF-κB activation and tumor growth, whereas its restoration rescued these effects. Clinically, E2F3, TRIM26, and phosphorylated p65 levels were positively correlated in PDAC tissues, and therapeutic delivery of siTRIM26 recapitulated NF-κB inhibition. These findings uncover an unrecognized E2F3-TRIM26-TAB1/TAK1-NF-κB signaling axis that links cell cycle regulation with inflammatory activation in PDAC and nominate TRIM26 as a druggable vulnerability to therapeutically decouple this oncogenic crosstalk. - Source: PubMed
Publication date: 2026/04/08
Zhang QiyueJing BopingRen DianyunSun YanCai HongkunLiang XueyiZhou YingkeWu HeshuiGuo Feng - Genome-wide association studies (GWASs) have identified hundreds of obesity-associated SNPs, but establishing their causality remains challenging. Here, we demonstrate that rs11676272, located in the ADCY3 gene, is a functional causal variant for obesity susceptibility. Bioinformatic analyses and dual-luciferase reporter assays indicate that the rs11676272 region may act as a human-gained enhancer regulating ADCY3 expression. In HEK293T cells, CRISPR-Cas9-mediated single-nucleotide editing of rs11676272 (T > C) reduces ADCY3 expression. Moreover, the rs11676272-T allele is preferentially bound by the transcription factor E2F3 to upregulate ADCY3 expression, whereas the rs11676272-C risk allele loses this binding. In vivo, the rs11676272 T > C variant in human ADCY3 (hADCY3) knock-in mice accelerates weight gain under high-fat diet conditions and shortens primary cilia in the ventromedial hypothalamus (VMH). CRISPRa-mediated activation of the hADCY3 promoter region rescues ciliary length in both the VMH and hypothalamic arcuate nucleus of Mut-hADCY3 mice. Our data reveal a causal role for rs11676272 in obesity, offering insight into potential therapeutic strategies. - Source: PubMed
Publication date: 2026/04/06
Wang WeinaLi YueDong ShengLiu YuweiGuo ChenghangSu YuzheTian WeiHu XiaoyuWang Zhenshan