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Post‐translational modification of forkhead family transcription factor, FoxO1, is an important regulatory mode for its diverse activities. FoxO1 is acetylated by HAT coactivators and its transcriptional activity is decreased via reduced DNA binding affinity. Here, we report that SET/TAF‐Iβ inhibited p300‐mediated FoxO1 acetylation in an INHAT domain‐dependent manner. SET/TAF‐Iβ interacted with FoxO1 and activated transcription of FoxO1 target gene, p21. Moreover, SET/TAF‐Iβ inhibited acetylation of FoxO1 and increased p21 transcription induced by oxidative stress. Our results suggest that SET/TAF‐Iβ inhibits FoxO1 acetylation and activates its transcriptional activity toward p21.SET/TAF‐Iβ inhibits FoxO1 acetylation. SET/TAF‐Iβ interacts with FoxO1 in INHAT domain dependent manner. Recruitment of FoxO1 on p21 promoter is increased by SET/TAF‐Iβ. SET/TAF‐Iβ induces p21 transcription and apoptosis under oxidative stress. [ABSTRACT FROM AUTHOR]

Highlights: [•] G9a upregulates p21 expression independently of its HMTase activity. [•] Positive regulation of p21 by G9a is p53 independent. [•] G9a interacts with PCAF to activate p21 expression. [•] G9a and PCAF are recruited to p21 promoter upon etoposide treatment. [•] G9a inhibits cell survival via p21-mediated apoptosis upon cellular stress. [ABSTRACT FROM AUTHOR]