EBF2 links KMT2D-mediated H3K4me1 to suppress pancreatic cancer progression via upregulating KLLN [ChIP-seq]
ChIP-seq revealed a strong reduction of KMT2D, H3K4me1 and EBF2 signals at the transcription start site (TSS) and promoter regions of genes that were downregulated in KMT2D-depleted (KMT2D-KD) cells Overall design: Chromatin immunoprecipitation DNA-sequencing (ChlP-seq) for KMT2D, EBF2 as well as the histone modifications H3K4me1 in negative control and KMT2D knowndown SW1990 cells.