Epigenome: H3K9 demethylase KDM3A potentiates interferon signaling and macrophage-driven inflammation in atherosclerosis

This repository contains raw and processed ChIPseq (KDM3A-HA and H3K27ac) and ATAC data generated to characterize transcriptional differences between wild-type or Kdm3a-/- RAW264.7 macrophages, in presence and absence of lipopolysaccharide. RAW264.7 cells were maintained in DMEM supplemented with 2mM L-glutamine, penicillin (100U/mL), streptomycin (100U/mL) and 10% fetal calf serum. All supplements are from Gibco, Life Technologies. Cells were cultures in humidified atmosphere with 5% CO2 at 37C. Kdm3a-/- RAW264.7 cells were generated using CRISPR/Cas9, targeting exon 4 with a gRNA integrated in pX330(Addgene #42230). RAW264.7 cells expressing KDM3A-HA were generated using a CRISPR HDR approach. Homology arms (~500 bp) targeting the final exon of Kdm3a were cloned into a donor plasmid. A Cas9-induced cut near the stop codon was introduced using a guide RNA, and all constructs were sequence-verified. The donor and CRISPR plasmids were co-transfected into cells, followed by puromycin selection and isolation of individual clones. Successful integration was confirmed by sequencing the targeted genomic region. When stimulated, lipopolysaccharide (B5,Sigma) was provided at 100ng/mL for RAW264.7. These data include: single-end sequencing fastq.gz paired-end sequencing fastq.gz KDM3A-HA peak files Metadata