GSE118576
Loss of Kat2a enhances transcriptional noise and depletes acute myeloid leukemia stem-like cells [ChIP-Seq]
Identification of histone acetylation targets of Kat2a activity in murine models of acute myeloid leukemia (AML) driven by the MLL-AF9 oncogenic fusion Overall design: Pooled mouse bone marrow (BM) samples obtained from terminal primary MLL-AF9 AMLs established from Kat2a WT (Mx1-Cre NEG = label NEG) or Kat2a KO (Mx1-Cre POS = label POS) cells were analysed for H3K9 and H3K27 acetylation marks, as well as for H3K4me3 (marking active promoters) and H3K4me1 (marking enhancers). Experiments were performed in duplicate (R1 and R2), as independent cell samples and chromatin preparations from the same pools of animals.