• Broach, James (PI)
  • Levine, Arnold (PI)
  • Shenk, Thomas (PI)
  • Zakian, Virginia A. (PI)
  • Schupbach, Gertrud M. (PI)
  • Schwarzbauer, Jean (PI)
  • Wieschaus, Eric (PI)

Project: Research project


The overall goal is to elucidate the mechanism whereby specific oncogenes
contribute to the subversion of a cell from normal growth to transformed
behavior. Oncogene function will be investigated at the molecular,
cellular and whole organism level. The research emphasis of component
projects are as follow: Subproject 1. Shenk will study the mechanism of adenovirus E1B
transforming protein action. He will also explore the mechanism whereby
adeno-associated virus inhibits the oncogenic activity of adenoviruses. Subproject 2. Flint will identify cellular and viral proteins and/or
nucleic acids with which the adenovirus E1A and E1B transforming proteins
interact. She will also employ recombinant retroviruses as vectors to
introduce individual adenovirus proteins into mammalian cells to probe
their individual activities. Subproject 3. Cole and Silver will map the chromosomal location of genes
which determine resistance or susceptibility to plasmacytoma induction in
the mouse, and then attempt to clone the relevant genetic loci. They will
also employ a recombinanat retrovirus carrying the murine c-myc gene to
study strain specificity of plasmacytoma induction. Subproject 4. Broach will conduct a genetic and physiological study of the
yeast RAS 1 and RAS 2 genes to determine the role these genes play in the
normal growth of a single eukaryotic cell. Subproject 5. Levine will utilize a cloned, murine p53 cDNA to study the
structure, function and regulation of the p53 cellular tumor antigen.
Levine and Gilboa will construct recombinant retroviruses which contain and
express the murine p53 gene. Levine and Schedl will investigate Drosophila
sequences which show strong homology to the murine p53 gene. Subproject 6. Hogan will employ photochemical probes to explore site
specific variation of DNA structure within the transcriptional control
regions of the adenovirus E1A and mouse c-myc genes. He will attempt to
relate structure variation to control of E1A and c-myc expression.
Effective start/end date7/1/862/28/07


  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health


Signal Transduction
nutrient availability
ras Proteins
cell growth
Cell Cycle
ras Guanine Nucleotide Exchange Factors
Cell Proliferation
Second Messenger Systems
Phosphoric Monoester Hydrolases
Protein Kinases
Phosphoprotein Phosphatases
immunosuppressive agents