GSE95712
Bmal1 regulates inflammatory response in macrophage
Deletion of Arntl disrupted temporal inflammatory response in macrophage. Mechanistically, the acetylation status of lysine 27 of histone 3 (H3K27ac) was enhanced at the PU.1-containing enhancers in Arntl-/- macrophages compared to the wild-type cells. Collectively, transcription factor network containing Bmal1 controls temporal inflammatory response of macrophages by regulating epigenetic states of enhancers. Overall design: Genome wide localization of Transcription factor Bmal1, NFkB (p65) and acetylation status of lysine 27 of histone 3 (H3K27ac) were assessed by ChIP-Seq.  Genome-wide  gene expression were analyzed by RNA-seq at indicated timepoints in the course of inflammatory response in primary macrophages.