NF-κB signaling is activated in AML1-deficient cells. (A) Schematic representation of the gene expression analysis. LSK cells from AML1 cKO mice (AML1 f/f) were transduced CreER-GFP or GFP expressing retroviruses. GFP+ cells were sorted and were subjected to gene expression analysis 24 or 48 hours after adding 4-OHT. (B) PCR genotyping of BM cells from AML1 cKO mice after adding 4-OHT. (C-I) NF-κB–related gene sets enriched in AML1-defecient cells (AML1 flox/flox, CreER+ 24 and 48 hours after adding 4-OHT) by GSEA Version 2.0. (C) A gene set that includes genes up-regulated by NF-κB (HINATA_NFKB_UP). (D) A gene set that includes genes which are up-regulated TNF-α treatment (TNFA_NFKB_DEP_UP). (E) A gene set that includes Ras-inducible, NF-κB–regulated genes (HANSON_NFKAPPB_IND). (F) A gene set that includes genes with promoter regions containing REL motif (V$CREL_01); (G) a gene set which includes Genes with promoter regions containing p65 motif (V$NFKAPPAB65_01). (H) A gene set that includes genes with promoter regions containing NF-κB motif ($NFKB_Q6). (I) Target genes of NF-κB.²¹  Nominal P value was estimated by GSEA software. (J) mRNA expression for NF-κB target genes in LSK cells transduced with CreER or mock from AML1 f/f mice 24 or 48 hours after 4-OHT addition. Error bars show mean ± SEM.