GSE114023
ChIP-seq data for H3K27 acetylation from 7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKKß
We found genetic deletion of IKKß in mdx cardiomyocytes improved cardiac function and normalized calcium transients, and that differential gene expression favored a repressive function for NF-[kappa]B in these mice. We suspected that NF-[kappa]B was conferring a more restrictive chromatin conformation in a subset of genes. ChIP-seq was performed for H3K27 acetylation to show this repressive function for NF-[kappa]B was a global effect and to identify specific genes with more permissive chromatin conformation in hearts of mdx mice with IKKß-deficient cardiomyocytes compared to mdx mice with intact IKKß signaling. Overall design: mdx mice conditionally deleted for IKKß specifically in cardiomyocytes were created crossing IKKß floxed mdx mice with mdx mice positive for the alpha myosin heavy chain (Myh6) promoter driving cre recombinase. Myh6 cre positive was our experimental condition and denoted “mdx heart Myh6-cre;IKKß[delta]. An age matched littermate without the cardiac-specific Myh6 cre was our control and denoted “mdx heart IKKßf/f”. ChIP was performed on whole hearts using an H3K27 acetylation antibody.