Project description:Using genetically engineered mice, overexpressing SRC-2, specifically in the prostate epithelium of PTEN heterozygous mice accelerates PTEN mutation induce tumor progression and develops a metastasis-prone cancer. Here we used ChIP-Seq analysis to identify genome-wide SRC-2 binding sites in mouse prostate. Examination of genome-wide SRC-2 binding in mouse prostate by ChIP-seq analysis. Samples were collected from pooled dorsal-lateral prostates of 7 months old-PTEN flox/+; Rosa26-SRC-2 OE/+ mice. Flash frozen tissues were then sent to Active Motif, Inc. for chromatin extraction and followed by immunoprecipitation using anti-SRC-2 antibody (A300-346A, Bethyl Lab., Inc.).
Project description:Using genetically engineered mice, overexpressing SRC-2, specifically in the prostate epithelium of PTEN heterozygous mice accelerates PTEN mutation induce tumor progression and develops a metastasis-prone cancer. Here we used ChIP-Seq analysis to identify genome-wide SRC-2 binding sites in mouse prostate.
Project description:We futher characterized genome-wide chromatin accessibility of WT and SRC-2-/- mouse liver at CT10 through DNase-Seq. In addition,chromatin accessibility was significantly reduced in SRC-2-/- mouse liver compared to WT mice at CT10. DNase-Seq was carried out in WT and SRC-2-/- mice in liver at CT10 using two doses of DNaseI.
Project description:We futher characterized genome-wide chromatin accessibility of WT and SRC-2-/- mouse liver at CT10 through DNase-Seq. In addition,chromatin accessibility was significantly reduced in SRC-2-/- mouse liver compared to WT mice at CT10.