Transcription Factor DP1

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  Subject Areas on Research

  • 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 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 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. 
  • 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. 
  • Collaborative role of E2F transcriptional activity and G1 cyclindependent kinase activity in the induction of S phase. 
  • Domains of the adenovirus E1A protein required for oncogenic activity are also required for dissociation of E2F transcription factor complexes. 
  • E2F transcription factor is a target for the RB protein and the cyclin A protein. 
  • 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. 
  • 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. 
  • 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. 
  • Functional properties of a Drosophila homolog of the E2F1 gene. 
  • 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. 
  • 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. 
  • Myc and Ras collaborate in inducing accumulation of active cyclin E/Cdk2 and E2F. 
  • Oncogenic capacity of the E2F1 gene. 
  • Regulation of the cyclin E gene by transcription factor E2F1. 
  • Role of the Rb/E2F pathway in cell growth control. 
  • Small contribution of G1 checkpoint control manipulation to modulation of p53-mediated apoptosis. 
  • The E2F transcription factor is a cellular target for the RB protein. 
  • 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. 
  • Use of the E2F transcription factor by DNA tumor virus regulatory proteins.