Project description:Using ChIP-seq technology, we tried to find out the whole genome targets for IRF2 in mouse colorectal cancer (CRC) cells. More than 7000 genes were defined as the target of IRF2.
Project description:Genome wide identification of TBX1 sites of occupancy in thyroid cancer cell line BCPAP cells by comparing control BCPAP cells transfected with pcDNA3.1-Vector (cotains Myc tag) with cells transfected with pcDNA3.1-TBX1 (contains Myc tag). By obtaining over 30 Million bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of TBX1 transfected. We find that transcription factor TBX1 exerts tumor suppressive properties through regulating multiple downstream targets involved in PI3K/Akt and MAPK/Erk signaling pathways.
Project description:To examine whether IRF2, a negative regulator of IFN signaling, constitutively represses IFN signaling by binding IFN-inducible gene loci in ISCs, we performed a genome-wide chromatin immunoprecipitation/DNA sequencing (ChIP-Seq) analysis of IRF2 in Lgr5 ISCs. We identified 381 binding peaks in these cells, including well-known IFN-inducible genes. Motif analysis showed significant enrichment of consensus-binding motifs for IRF transcription factors within these peaks. Within IRF2-occupied genes in ISCs, we identified 204 of experimentally validated IFN-inducible genes from Interferome database, and 10.8% of them were overlapped with the genes upregulated by type I IFN stimulation in ISCs. These findings indicated for the first time that IRF2 constitutively bound and repressed the sterile IFN signaling at the level of ISCs.