Project description:Using ATAC-seq, we examined genome-wide chromatin accessibility in the MOLM13 and MV4;11 human MLL-fusion acute myeloid leukemia cell lines.
Project description:Using DNaseI hypersensitivity (HS) assays (Dnase-seq), high resolution DNaseI digestion profiles were generated genome-wide in diverse human cell types. We showed that within general regions of DNaseI HS that are known to identify locations of gene regulatory elements, DNaseI digestion patterns allowed us to identify locations of individual transcription factor binding sites that protected against the bound DNA against digestion. To measure the accuracy of these footprints, we also generated ChIP-seq data for the CTCF DNA binding factor in the same cell growths. We found that DNaseI footprints containing the CTCF canonical binding motif show significant ChIP-seq signal while CTCF binding motifs not in footprints show almost no signal providing one measure of valdation of the DNaseI footprints. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Six cell lines representing cervica carcinoma, chronic myeloid leukemia, human embryonic stem cells, lymphoblastoid cells, human epidermal keratinocytes and umbilical vein endothelial cells were analyzed using Dnase-seq.
Project description:Using DNaseI hypersensitivity (HS) assays (Dnase-seq), high resolution DNaseI digestion profiles were generated genome-wide in diverse human cell types. We showed that within general regions of DNaseI HS that are known to identify locations of gene regulatory elements, DNaseI digestion patterns allowed us to identify locations of individual transcription factor binding sites that protected against the bound DNA against digestion. To measure the accuracy of these footprints, we also generated ChIP-seq data for the CTCF DNA binding factor in the same cell growths. We found that DNaseI footprints containing the CTCF canonical binding motif show significant ChIP-seq signal while CTCF binding motifs not in footprints show almost no signal providing one measure of valdation of the DNaseI footprints. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Five cell lines representing cervica carcinoma, chronic myeloid leukemia, embryonic stem cells, epidermal keratinocytes, and umbilical vein endothelial cells were analyzed using ChIP-seq.
Project description:We performed ChIP-seq to identify genome-wide REST (NRSF) binding in the human CD4+ T cells. The data were compared to REST occupancy in additional 15 human cell types analyzed by the ENCODE project (GSE32465) in order to study the dynamics and context-dependent functions of REST-chromatin interaction. Identification of REST binding by ChIP-seq in human CD4+ T cells.
Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin. Identification of genomic p53 binding sites in HCT116 cells by ChIP-seq.
Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated withionizing radiation