E2F Transcription Factors
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Subject Areas on Research
- A bistable Rb-E2F switch underlies the restriction point.
- 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.
- Bimodular auxin response controls organogenesis in Arabidopsis.
- Cdc6 is regulated by E2F and is essential for DNA replication in mammalian cells.
- 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.
- 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.
- 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.
- 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.
- Role for E2F in control of both DNA replication and mitotic functions as revealed from DNA microarray analysis.
- 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.
- Therapeutic applications of transcription factor decoy oligonucleotides.
- 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 Professor of Gynecologic Oncology, Obstetrics and Gynecology, Gynecologic Oncology