Transcription Factor DP1

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  Subject Areas on Research

  • A gene therapy strategy using a transcription factor decoy of the E2F binding site inhibits smooth muscle proliferation in vivo. 
  • 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 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. 
  • Cdc6 is regulated by E2F and is essential for DNA replication in mammalian cells. 
  • Cell cycle: Flies teach an old dogma new tricks. 
  • 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. 
  • 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. 
  • 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. 
  • Small contribution of G1 checkpoint control manipulation to modulation of p53-mediated apoptosis. 
  • Therapeutic applications of transcription factor decoy oligonucleotides.