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Research was conducted to test whether the tumor suppressor gene product , p19(super Arf) hinders oncogenic transformation in primary cells and whether its role is abrogated when p53 is neutralized by viral oncoproteins and dominant-negative mutants. Cell cultures were monitored and maintained by calcium phosphate using the same amounts of DNA as in p53 degradation. Results showed high levels of genetic instability in p53 and that potent tumor suppressor activity resulted from the encoding of unrelated antioncogenic proteins with cooperating modes of action.

It has been possible to use yeast two-hybrid interaction screens and immunoprecipitation assays to identify possible effectors of mSin3 transcriptional repression function. This research has allowed the characterization of an interaction between mSin3 and the co-repressor N-CoR protein. This has been shown to be required for mSin3-mediated repression of basal transcription. It is likely that multiple co-repressors jointly prompt repression mediated by a single DNA-binding transcription factor.