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      Cellular targets for activation by the E2F1 transcription factor include DNA synthesis- and G1/S-regulatory genes.

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      Molecular and Cellular Biology
      American Society for Microbiology

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          Abstract

          Although a number of transfection experiments have suggested potential targets for the action of the E2F1 transcription factor, as is the case for many transcriptional regulatory proteins, the actual targets in their normal chromosomal environment have not been demonstrated. We have made use of a recombinant adenovirus containing the E2F1 cDNA to infect quiescent cells and then measure the activation of endogenous cellular genes as a consequence of E2F1 production. We find that many of the genes encoding S-phase-acting proteins previously suspected to be E2F targets, including DNA polymerase alpha, thymidylate synthase, proliferating cell nuclear antigen, and ribonucleotide reductase, are indeed induced by E2F1. Several other candidates, including the dihydrofolate reductase and thymidine kinase genes, were only minimally induced by E2F1. In addition to the S-phase genes, we also find that several genes believed to play regulatory roles in cell cycle progression, such as the cdc2, cyclin A, and B-myb genes, are also induced by E2F1. Moreover, the cyclin E gene is strongly induced by E2F1, thus defining an autoregulatory circuit since cyclin E-dependent kinase activity can stimulate E2F1 transcription, likely through the phosphorylation and inactivation of Rb and Rb family members. Finally, we also demonstrate that a G1 arrest brought about by gamma irradiation is overcome by the overexpression of E2F1 and that this coincides with the enhanced activation of key target genes, including the cyclin A and cyclin E genes.

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          Author and article information

          Journal
          Molecular and Cellular Biology
          Mol. Cell. Biol.
          American Society for Microbiology
          0270-7306
          1098-5549
          August 01 1995
          August 1995
          August 1995
          August 01 1995
          : 15
          : 8
          : 4215-4224
          Article
          10.1128/MCB.15.8.4215
          230660
          7623816
          5f7c65ac-c8df-4741-bee4-830dd94d5895
          © 1995
          History

          Molecular medicine,Neurosciences
          Molecular medicine, Neurosciences

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