E2F Transcription Factors

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  Subject Areas on Research

  • A bistable Rb-E2F switch underlies the restriction point. 
  • A combinatorial mechanism for determining the specificity of E2F activation and repression. 
  • A gene therapy strategy using a transcription factor decoy of the E2F binding site inhibits smooth muscle proliferation in vivo. 
  • A genomic strategy to elucidate modules of oncogenic pathway signaling networks. 
  • A mechanism of COOH-terminal binding protein-mediated repression. 
  • A noncanonical role for the CKI-RB-E2F cell-cycle signaling pathway in plant effector-triggered immunity. 
  • Adenovirus E1A, simian virus 40 tumor antigen, and human papillomavirus E7 protein share the capacity to disrupt the interaction between transcription factor E2F and the retinoblastoma gene product. 
  • An integrated genomic-based approach to individualized treatment of patients with advanced-stage ovarian cancer. 
  • An oligonucleotide decoy for transcription factor E2F inhibits mesangial cell proliferation in vitro. 
  • Aromatic hydrocarbon receptor interaction with the retinoblastoma protein potentiates repression of E2F-dependent transcription and cell cycle arrest. 
  • Balancing the decision of cell proliferation and cell fate. 
  • Bimodular auxin response controls organogenesis in Arabidopsis. 
  • Cdc6 is regulated by E2F and is essential for DNA replication in mammalian cells. 
  • Cell cycle: Flies teach an old dogma new tricks. 
  • Distinct roles of E2F proteins in vascular smooth muscle cell proliferation and intimal hyperplasia. 
  • Distinctions in the specificity of E2F function revealed by gene expression signatures. 
  • Domains of the adenovirus E1A protein required for oncogenic activity are also required for dissociation of E2F transcription factor complexes. 
  • Drosophila E2f2 promotes the conversion from genomic DNA replication to gene amplification in ovarian follicle cells. 
  • E2F4-RB and E2F4-p107 complexes suppress gene expression by transforming growth factor beta through E2F binding sites. 
  • Efficacy and safety of edifoligide, an E2F transcription factor decoy, for prevention of vein graft failure following coronary artery bypass graft surgery: PREVENT IV: a randomized controlled trial. 
  • Endothelial healing in vein grafts: proliferative burst unimpaired by genetic therapy of neointimal disease. 
  • Ex-vivo gene therapy of human vascular bypass grafts with E2F decoy: the PREVENT single-centre, randomised, controlled trial. 
  • Expression of the E2F1 transcription factor overcomes type beta transforming growth factor-mediated growth suppression. 
  • Gene expression phenotypic models that predict the activity of oncogenic pathways. 
  • Gene therapy with an E2F transcription factor decoy inhibits cell cycle progression in rat anti-Thy 1 glomerulonephritis. 
  • Highly coordinated gene regulation in mouse skeletal muscle regeneration. 
  • IFN-α inhibits telomerase in human CD8⁺ T cells by both hTERT downregulation and induction of p38 MAPK signaling. 
  • Identification of E2F target genes that are rate limiting for dE2F1-dependent cell proliferation. 
  • Inhibition of cell proliferation by an RNA ligand that selectively blocks E2F function. 
  • Inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway induces p53-independent transcriptional regulation of p21(WAF1/CIP1) in human prostate carcinoma cells. 
  • Isolation and initial characterization of the BRCA2 promoter. 
  • Long-term stabilization of vein graft wall architecture and prolonged resistance to experimental atherosclerosis after E2F decoy oligonucleotide gene therapy. 
  • Myc requires distinct E2F activities to induce S phase and apoptosis. 
  • Network calisthenics: control of E2F dynamics in cell cycle entry. 
  • Optimizing aptamer activity for gene therapy applications using expression cassette SELEX. 
  • Origin of bistability underlying mammalian cell cycle entry. 
  • Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles. 
  • Role for E2F in control of both DNA replication and mitotic functions as revealed from DNA microarray analysis. 
  • Selective induction of E2F1 in response to DNA damage, mediated by ATM-dependent phosphorylation. 
  • Small contribution of G1 checkpoint control manipulation to modulation of p53-mediated apoptosis. 
  • Stochastic E2F activation and reconciliation of phenomenological cell-cycle models. 
  • Tension and robustness in multitasking cellular networks. 
  • The ABL2 kinase regulates an HSF1-dependent transcriptional program required for lung adenocarcinoma brain metastasis. 
  • The E2F1-3 transcription factors are essential for cellular proliferation. 
  • Therapeutic applications of transcription factor decoy oligonucleotides. 
  • Transcriptional repressor functions of Drosophila E2F1 and E2F2 cooperate to inhibit genomic DNA synthesis in ovarian follicle cells. 
  • Transforming growth factor beta-mediated transcriptional repression of c-myc is dependent on direct binding of Smad3 to a novel repressive Smad binding element. 
  • Vitamin E succinate inhibits human prostate cancer cell growth via modulating cell cycle regulatory machinery. 
  • Yin yang 1 modulates taxane response in epithelial ovarian cancer. 
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  Keywords of People

  • Alexander, John Hunter Peel, Professor of Medicine, Medicine, Cardiology
  • Berchuck, Andrew, James M. Ingram Distinguished Professor of Gynecologic Oncology, Obstetrics and Gynecology, Gynecologic Oncology