A lentiviral vector with expression controlled by E2F-1: a potential tool for the study and treatment of proliferative diseases.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read More Add to Saved list
  • Author(s): Strauss BE;Strauss BE; Patrício JR; de Carvalho AC; Bajgelman MC
  • Source:
    Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2006 Oct 06; Vol. 348 (4), pp. 1411-8. Date of Electronic Publication: 2006 Aug 10.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print-Electronic Cited Medium: Print ISSN: 0006-291X (Print) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE
    • Publication Information:
      Publication: <2002- >: San Diego, CA : Elsevier
      Original Publication: New York, Academic Press.
    • Subject Terms:
      Gene Expression Regulation* ; Genetic Vectors*; E2F1 Transcription Factor/*genetics ; Lentivirus/*genetics; Animals ; Cell Cycle ; Cell Proliferation ; Cells, Cultured ; E2F Transcription Factors/metabolism ; Genes, Reporter ; Genes, Tumor Suppressor ; Genetic Therapy ; Humans ; Promoter Regions, Genetic ; Rats
    • Abstract:
      We have constructed a lentiviral vector with expression limited to cells presenting active E2F-1 protein, a potential advantage for gene therapy of proliferative diseases. For the FE2FLW vector, the promoter region of the human E2F-1 gene was utilized to drive expression of luciferase cDNA, included as a reporter of viral expression. Primary, immortalized, and transformed cells were transduced with the FE2FLW vector and cell cycle alterations were induced with serum starvation/replacement, contact inhibition or drug treatment, revealing cell cycle-dependent changes in reporter activity. Forced E2F-1 expression, but not E2F-2 or E2F-3, increased reporter activity, indicating a major role for this factor in controlling expression from the FE2FLW virus. We show the utility of this vector as a reporter of E2F-1 and proliferation-dependent cellular alterations upon cytotoxic/cytostatic treatment, such as the introduction of tumor suppressor genes. We propose that the FE2FLW vector may be a starting point for the development of gene therapy strategies for proliferative diseases, such as cancer or restinosis.
    • Accession Number:
      0 (E2F Transcription Factors)
      0 (E2F1 Transcription Factor)
      0 (E2F1 protein, human)
    • Publication Date:
      Date Created: 20060822 Date Completed: 20061019 Latest Revision: 20121115
    • Publication Date:
      20231215
    • Accession Number:
      10.1016/j.bbrc.2006.08.007
    • Accession Number:
      16920066