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 cyclin A-protein kinase complex possesses sequence-specific DNA binding activity: p33cdk2 is a component of the E2F-cyclin A complex. 
  • A gene therapy strategy using a transcription factor decoy of the E2F binding site inhibits smooth muscle proliferation in vivo. 
  • A genetic analysis of the E2F1 gene distinguishes regulation by Rb, p107, and adenovirus E4. 
  • 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. 
  • A role for Mediator complex subunit MED13L in Rb/E2F-induced growth arrest. 
  • A role for Myc in facilitating transcription activation by E2F1. 
  • A role for a bent DNA structure in E2F-mediated transcription activation. 
  • A unique role for the Rb protein in controlling E2F accumulation during cell growth and differentiation. 
  • 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. 
  • Adenovirus E1A: transcription regulation and alteration of cell growth control. 
  • 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. 
  • Autoregulatory control of E2F1 expression in response to positive and negative regulators of cell cycle progression. 
  • 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 regulation of the E2F transcription factor involves an interaction with cyclin A. 
  • Cell cycle targets of the DNA tumor viruses. 
  • Cell cycle: Flies teach an old dogma new tricks. 
  • Cellular targets for activation by the E2F1 transcription factor include DNA synthesis- and G1/S-regulatory genes. 
  • Collaborative role of E2F transcriptional activity and G1 cyclindependent kinase activity in the induction of S phase. 
  • Combinatorial gene control involving E2F and E Box family members. 
  • Conservation and divergence of C-terminal domain structure in the retinoblastoma protein family. 
  • Disruption of cell-cycle control by viral oncoproteins. 
  • Distinct mechanisms control the accumulation of the Rb-related p107 and p130 proteins during cell growth. 
  • Distinct roles for E2F proteins in cell growth control and apoptosis. 
  • 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. 
  • E2F transcription factor is a target for the RB protein and the cyclin A protein. 
  • E2F-1 accumulation bypasses a G1 arrest resulting from the inhibition of G1 cyclin-dependent kinase activity. 
  • E2F1 overexpression in quiescent fibroblasts leads to induction of cellular DNA synthesis and apoptosis. 
  • E2F1-specific induction of apoptosis and p53 accumulation, which is blocked by Mdm2. 
  • E2F1: a magic bullet for atherosclerosis? 
  • E2F4-RB and E2F4-p107 complexes suppress gene expression by transforming growth factor beta through E2F binding sites. 
  • E2F: a link between the Rb tumor suppressor protein and viral oncoproteins. 
  • E2Fs link the control of G1/S and G2/M transcription. 
  • Ectopic E2F expression induces S phase and apoptosis in Drosophila imaginal discs. 
  • 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. 
  • Expression of the HsOrc1 gene, a human ORC1 homolog, is regulated by cell proliferation via the E2F transcription factor. 
  • Expression of transcription factor E2F1 induces quiescent cells to enter S phase. 
  • Functional analysis of E2F transcription factor. 
  • Functional properties of a Drosophila homolog of the E2F1 gene. 
  • 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. 
  • Identification of distinct roles for separate E1A domains in disruption of E2F complexes. 
  • Induction of DNA replication in adult rat neurons by deregulation of the retinoblastoma/E2F G1 cell cycle pathway. 
  • Inhibition of cell proliferation by an RNA ligand that selectively blocks E2F function. 
  • Inhibition of cyclin D-CDK4/CDK6 activity is associated with an E2F-mediated induction of cyclin kinase inhibitor activity. 
  • 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. 
  • Interaction of YY1 with E2Fs, mediated by RYBP, provides a mechanism for specificity of E2F function. 
  • Interactions of the p107 and Rb proteins with E2F during the cell proliferation response. 
  • 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. 
  • MicroRNA-mediated positive feedback loop and optimized bistable switch in a cancer network Involving miR-17-92. 
  • Myc and Ras collaborate in inducing accumulation of active cyclin E/Cdk2 and E2F. 
  • Myc requires distinct E2F activities to induce S phase and apoptosis. 
  • Network calisthenics: control of E2F dynamics in cell cycle entry. 
  • Noise propagation in gene regulation networks involving interlinked positive and negative feedback loops. 
  • Oncogenic capacity of the E2F1 gene. 
  • Optimizing aptamer activity for gene therapy applications using expression cassette SELEX. 
  • Origin of bistability underlying mammalian cell cycle entry. 
  • Patterns of cell signaling pathway activation that characterize mammary development. 
  • Regulation of the cyclin E gene by transcription factor E2F1. 
  • Role for E2F in control of both DNA replication and mitotic functions as revealed from DNA microarray analysis. 
  • Role of the Rb/E2F pathway in cell growth control. 
  • Selective induction of E2F1 in response to DNA damage, mediated by ATM-dependent phosphorylation. 
  • Signaling networks that link cell proliferation and cell fate. 
  • Small contribution of G1 checkpoint control manipulation to modulation of p53-mediated apoptosis. 
  • Specificity in the activation and control of transcription factor E2F-dependent apoptosis. 
  • Stochastic E2F activation and reconciliation of phenomenological cell-cycle models. 
  • Temporal control of cell cycle gene expression mediated by E2F transcription factors. 
  • Tension and robustness in multitasking cellular networks. 
  • The E2F transcription factor is a cellular target for the RB protein. 
  • The E2F1-3 transcription factors are essential for cellular proliferation. 
  • The Rb-related p107 protein can suppress E2F function independently of binding to cyclin A/cdk2. 
  • The Rb/E2F pathway and cancer. 
  • The accumulation of an E2F-p130 transcriptional repressor distinguishes a G0 cell state from a G1 cell state. 
  • The human cytomegalovirus IE1-72 protein interacts with the cellular p107 protein and relieves p107-mediated transcriptional repression of an E2F-responsive promoter. 
  • The interaction of RB with E2F coincides with an inhibition of the transcriptional activity of E2F. 
  • Therapeutic applications of transcription factor decoy oligonucleotides. 
  • Toward an understanding of the functional complexity of the E2F and retinoblastoma families. 
  • Transcriptional regulation. A closer look at E2F. 
  • 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. 
  • Use of the E2F transcription factor by DNA tumor virus regulatory proteins. 
  • 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