Missense mutations in the p53 coding gene cause loss and gain of function. We have identified a hotspot mutation, p53N236S , which results in the aggressive progression of tumorigenesis in a knock-in mouse model. To understand the biological significance of the p53N236S mutation, we performed ChIP-on-chip combined with microarray assay to profile the regulated gene expression pattern. We could classify the p53N236S mutant function into six categories. Among these, we reveal a new aspect of gain of function, the enhancement of wild-type p53 function, which has not been reported previously. We also show the existence of residual wild-type p53 function in p53N236S . Our data shed light on understanding the difference between this type of low-incidence hotspot p53 mutations and classical hotspot mutations.
Keywords: expression profile; gain of function; p53N236S; transcription profile.
© 2018 Federation of European Biochemical Societies.