Faina Vikhanskaya

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Tumour-derived p53 mutants are thought to have acquired 'gain-of-function' properties that contribute to oncogenicity. We have tested the hypothesis that p53 mutants suppress p53-target gene expression, leading to enhanced cellular growth. Silencing of mutant p53 expression in several human cell lines was found to lead to the upregulation of wild-type(More)
p73 is a member of the p53 family often overexpressed in human cancer. Its regulation, particularly following DNA damage, is different from that of p53. Following DNA damage, we found induction of p73 at both the protein and mRNA levels. Furthermore, by using different p73 promoter fragments, we found a role for E2F1 in mediating transcription of p73.(More)
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