H3K4methylation in Setd1a loss-of-function Raw264.7 cells upon LPS or Dex+LPS stimulation

Nuclear interaction studies by ChIP coupled with mass spectrometry identified the COMPASS/SETD1A complex as interaction partner of the glucocorticoid receptor (GR) in murine bone marrow-derived macrophages (BMDMs). Here, we profiled H3K4me1, H3K4me2 and H3K4me3 in wild-type and Setd1a hypermorphic (Setd1aDel/+) Raw264.7 cells after LPS and Dex+LPS stimulation by spike-in ChIP-Seq. Overall design: We profiled changes in H3K4me1, H3K4me2 and H3K4me3 in wild-type and Setd1aDel/+ (loss-of-function) Raw264.7 cells after challenge with LPS or Dex+LPS. All ChIP-Seq experiments were done in duplicates or more. We used Drosophila melanogaster chromatin as spike-in control.