Ontology highlight
ABSTRACT:
PROVIDER: PRJNA412794 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide identification of binding sites of Evi1 in human myeloid cell lines
2015-08-06 | E-GEOD-16238 | ExpressionAtlas
Project description:We report the application of genome-wide protein binding sites capture (GWPBS-Cap) technology for high-throughput profiling of protein binding sites in mammalian cells. By obtaining over 37 billion bases of sequence from NaCl washed chromatin DNA in each group, we got an unprecedented view into genome-wide binding patterns of many DNA binding proteins of Hela cells. We find that active promoters contain more PBSs with lower NaCl tolerance and our technology provides a genome-wide landscape of DNA-protein interactions.
2018-07-10 | GSE116770 | GEO
Project description:Epigenomics is developing a colon cancer screening assay based on differential methylation of specific CpG sites for the detection of early stage disease. A genome-wide methylation analysis and oligonucleotide array study using DNA from various stages of colon cancer and normal tissue have been completed to obtain candidate CpG markers. Based on results obtained in the above studies, Epigenomics has moved to the final stages of feasibility with a specific, highly sensitive real-time marker assay that is able to detect colon cancer DNA in blood plasma.
| 2056787 | ecrin-mdr-crc
Project description:We analyzed the overlap in genome wide binding sites between Jarid2 and Suz12 in mouse ES cells and find that Jarid2 and Suz12 peaks have an high degree (90%) of overlap. Moreover we analyzed the effect of Jarid2 down regulation on genome wide Suz12 binding sites and found that Loss of Jarid2 lead to the loss of 70% of Suz12 binding sites and to a 10 Fold reduction in intensity for 90% of Suz12 binding sites. Overall, these results demonstrate that Jarid2 plays an essential role for Suz12 (PRC2 complex) association to DNA. Examination of two different proteins in two different cell lines
2010-01-27 | E-GEOD-19365 | biostudies-arrayexpress
Project description:Analysis of PAX8 binding sites by chromatin immunoprecipitation coupled with ultra-high-throughput sequencing (ChIP-seq) in PCCL3 rat cells. Results provide insight into the contribution of this regulatory factor to transcription genome-wide. We generate a genome wide map of PAX8 binding sites in PCCL3 cells using as negative control an input DNA obtained just prior to Pax8 immunoprecipitation
2012-06-27 | E-GEOD-26871 | biostudies-arrayexpress
Project description:We analyzed the overlap in genome wide binding sites between Jarid2 and Suz12 in mouse ES cells and find that Jarid2 and Suz12 peaks have an high degree (90%) of overlap. Moreover we analyzed the effect of Jarid2 down regulation on genome wide Suz12 binding sites and found that Loss of Jarid2 lead to the loss of 70% of Suz12 binding sites and to a 10 Fold reduction in intensity for 90% of Suz12 binding sites. Overall, these results demonstrate that Jarid2 plays an essential role for Suz12 (PRC2 complex) association to DNA.
2010-01-27 | GSE19365 | GEO
Project description:We report that a DNA minor groove binding hairpin pyrrole-imidazole (Py-Im) polyamide interferes with RNA polymerase II (RNAP2) activity in cell culture. Genome-wide mapping of RNAP2 binding shows reduction of occupancy preferentially at transcription start sites (TSS), while occupancy at enhancer sites are is unchanged. Genome-wide mapping of RNA polymerase II in LNCaP cells treated with DHT and DHT with Py-Im polyamide.
2013-01-31 | E-GEOD-43253 | biostudies-arrayexpress
Project description:We report here genome-wide analysis of the tumor suppressor p53 binding sites in normal human cells. 743 high-confidence ChIP-seq peaks representing putative genomic binding sites were identified in normal IMR90 fibroblasts using a reference chromatin sample. More than 40 % were located within 2 kb of a transcription start site (TSS), a distribution similar to that documented for individually studied functional p53 binding sites and to date not observed by previous genome-wide studies. Nearly half of the high-confidence binding sites in the IMR90 cells reside in CpG islands, in marked contrast to sites reported in cancer-derived cells. The distinct genomic features of the IMR90 binding sites do not reflect a distinct preference for specific sequences, since the de novo developed p53 motif based on our study is similar to those reported by genome-wide studies of cancer cells. More likely the different chromatin landscape in normal compared to cancer-derived cells influences p53 binding via modulating availability of the sites. We compared the IMR90 ChIP-seq peaks to the recently published IMR90 methylome1, and demonstrated that they are enriched at hypomethylated DNA. Our study represents the first genome-wide, de novo mapping of p53 binding sites in normal human cells and reveals that p53 binding sites reside in distinct genomic landscapes in normal and cancer-derived human cells. Identification of genomic p53 binding sites in normal human cells by ChIP-seq.
2011-12-08 | E-GEOD-31558 | biostudies-arrayexpress
Project description:The genome wide ChIP-on-chip analysis to identify the DNA binding sites for the M.tuberculosis sigma factor Rv3286c (SigF)
2012-01-20 | GSE34919 | GEO
Project description:The NuRD complex is generally thought to repress transcription at both hyper- and hypomethylated regions in the genome. In addition, the complex is involved in the DNA damage response. Here, we show that ZMYND8 bridges NuRD to a number of putative DNA-binding zinc finger proteins. The ZMYND8 MYND domain directly interacts with PPPLΦ motifs in the NuRD subunit GATAD2A. Furthermore, GATAD2A and GATAD2B exclusively form homodimers and they thus define mutually exclusive NuRD subcomplexes. ZMYND8 and MBD3 share a large number of genome-wide binding sites, mostly active promoters and enhancers. Depletion of ZMYND8 does not affect NuRD occupancy genome-wide and expression of NuRD/ZMYND8 target genes in steady-state asynchronous cells. However, ZMYND8 facilitates immediate recruitment of GATAD2A/NuRD to induced sites of DNA damage in a PAR-dependent manner. These results thus show that a specific substoichiometric interaction with a NuRD subunit paralogue provides unique functionality to a distinct NuRD subcomplex.
2016-10-10 | PXD003856 | Pride