Project description:We mapped the genome-wide binding profiles of GR throughout the day/night cycle (ZT0-ZT4-ZT8-ZT12-ZT16-ZT20) by using ChIP-Seq in livers from control mice and mice fed High Fat Diet (HFD) for 12 weeks
Project description:We mapped the genome-wide binding profiles of GR throughout the day/night cycle (ZT0-ZT4-ZT8-ZT12-ZT16-ZT20) by using ChIP-Seq in livers from control mice and mice fed High Fat Diet (HFD) for 12 weeks
Project description:We mapped the genome-wide profiles of Histone H3K27 acetylation (two time points, ZT0 and ZT12) by using ChIP-Seq in livers from control mice and mice fed High Fat Diet (HFD) for 12 weeks
Project description:We mapped the genome-wide binding profiles of GR by using ChIP-Seq in livers from mice fed control or HFD diet after acute exogenous ligand (DEX) administration.
Project description:Genes with increased H3K27ac marks in their promoters were found in adult mice L4 vertebrae from mice using H3K27ac ChIP-Seq. Recent data suggests that in animals and humans that a maternal diet high in fat leads to poor bone growth and development in offspring. Genes with increased H3K27ac epigenetic marks normally have higher levels of expression. Understanding which genes are being upregulated due to maternal or offspring high fat diet would allow for better treatments to combat bone loss to be developed.
Project description:We performed ChIP-seq targeting the H3K27ac, H3K4me1, H3K27me3 and H3K9me3 in the U2OS-GR and U2OS-AR cell lines. The cell lines are derived from U2OS ATTC:HTB-96 and stably transfected with an expression construct for either rat GR or human AR, respectively. The U2OS-GR cells were treated with dexamethasone (1 µM) or vehicle (ethanol) for 90 minutes. The U2OS-AR cells were treated with R1881 (5 nM) or vehicle (DMSO) for 4 hours.
Project description:Genes with increased H3K27ac marks in their promoters were found in mice embryonic calvaria cells using H3K27ac ChIP-Seq. Recent data suggests that in animals and humans that a maternal diet high in fat leads to poor bone growth and development in offspring. Genes with increased H3K27ac epigenetic marks normally have higher levels of expression. Understanding which genes are being upregulated in the offspring due to maternal diet would allow for better treatments to combat bone loss to be developed.