Genome-wide profiling of Kdm2a binding and H3K36me2 of hypoxia-cultured B cells derived from miR-155-sufficient and -deficient mice [ChIP-seq]

To investigate the impact caused by miR-155 ablation, B cells from miR-155-sufficient and -deficient mice were cultured in hypoxic conditions and analyzed for profiling the binding of a miR-155 target, Kdm2a, to genomic loci and the distribution pattern of H3K36me2, which Kdm2a demethylates. Overall design: Splenic B cells derived from miR-155-sufficient or -deficient mice were cultured in hypoxic conditions.