Expression profiling by high throughput sequencing Genome binding/occupancy profiling by high throughput sequencing
Summary
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.
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