Wild‐type p53 functions as a tumour suppressor while mutant p53 functions as an oncogene. In this new study we propose that this switch depends on Δ160p53, the most conserved isoform of p53, which is overexpressed in p53 mutant cells.
Here is a video by leading author Marco explaining the importance of the findings:
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Cells carrying p53 mutations overexpress shorter p53 isoforms.
The Δ160p53 isoform possesses pro‐oncogenic potential similar to mutant p53.
“Gain‐of‐function” cancer phenotypes induced by mutant p53 depend on the expression of short p53 isoforms.