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The transcription and expression profile of p53 N236S mutant reveals new aspects of gain of function for mutant p53
Author(s) -
Wang Boyuan,
Dan Juhua,
Li Haili,
Hou Jing,
Shi Mingling,
Sanjay Kumar Singh,
Chang Jeffrey T.,
Luo Ying
Publication year - 2018
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13223
Subject(s) - mutant , biology , carcinogenesis , gain of function , wild type , missense mutation , gene , genetics , microbiology and biotechnology , cancer research , mutation
Missense mutations in the p53 coding gene cause loss and gain of function. We have identified a hotspot mutation, p53 N236S , which results in the aggressive progression of tumorigenesis in a knock‐in mouse model. To understand the biological significance of the p53 N236S mutation, we performed Ch IP ‐on‐chip combined with microarray assay to profile the regulated gene expression pattern. We could classify the p53 N236S 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 p53 N236S . Our data shed light on understanding the difference between this type of low‐incidence hotspot p53 mutations and classical hotspot mutations.