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KMT2C — TP53

Text-mined interactions from Literome

Lee et al., Proc Natl Acad Sci U S A 2009 (Cell Transformation, Neoplastic...) : Consistent with the in vivo observations, and the demonstration of a direct interaction between p53 and ASCOM, cell based assays have revealed that ASCOM , through ASC-2 and MLL3/4, acts as a p53 coactivator and is required for H3K4-trimethyation and expression of endogenous p53-target genes in response to the DNA damaging agent doxorubicin ... In support of redundant functions for MLL3 and MLL4 for some events, siRNA mediated down-regulation of both MLL3 and MLL4 is required to suppress doxorubicin-inducible expression of several p53-target genes
Kim et al., Mol Endocrinol 2011 : Requirement for MLL3 in p53 regulation of hepatic expression of small heterodimer partner and bile acid homeostasis ... Here, we show that the MLL3 complex is also essential for p53 transactivation of SHP ... For both HepG2 cells and mouse liver, we also demonstrate that p53 directs the recruitment of different components of the MLL3 complex to the p53-response elements of SHP and that p53 dependent H3-lysine-4-trimethylation of SHP requires MLL3