Moreover, we found that the increase in the acetylation level of the K382 site of p53R181C induced by H 2 O 2 stimulation was not as significant as that of the wild type in H1299 cells which are p53-null (Fig. 2G ).
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The p53 R181C mutation accumulates through impaired deacetylation by Sirt1 and facilitates tumor development.
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