ChIP-seq analysis of CCCTC-binding factor (CTCF) binding in livers of C3H mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB54882 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9976330.fastq.gz | Fastqsanger.gz | |||
| ERR9976340_1.fastq.gz | Fastqsanger.gz | |||
| ERR9976340_2.fastq.gz | Fastqsanger.gz | |||
| ERR9976350_1.fastq.gz | Fastqsanger.gz | |||
| ERR9976350_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 54 |
Similar Datasets
Project description:This study aims to investigate the interactions of mutagenic lesions from diethylnitrosamine (DEN) treatment of mouse livers with such processes as replication, transcription, and interaction of DNA with proteins. Liver samples of 15-day old (P15) untreated C3H/HeOuJ mice were isolated and flash-frozen. ChIP-seq was performed to identify CTCF binding sites in livers of ten pooled individuals. The experiment was done with five biological replicates with a matched input library.
2023-04-29 | E-MTAB-11959 | biostudies-arrayexpress
Project description:ChIP-Seq analysis of CCCTC-binding factor (CTCF) binding in rodents
| PRJEB21041 | ENA
Project description:The mammalian CCCTC-binding factor (CTCF) regulates gene expression through the formation of higher order chromatin structures. Recent evidence has implicated a role for CTCF in regulating gene expression in the human MHCII locus. To investigate the role of CTCF in murine MHCII gene expression we mapped CTCF binding sites in B cells (MHCII+ cells) and Plasmablasts which are differentiated B cells that have silenced MHCII gene expression. These observations lead to the identification of differential CTCF binding during differentiation in these cell types and suggest mechanims of MHCII gene regulation. Comparison of CTCF binding in B cells and Plasmablasts in mice using ChIP-seq
2014-02-05 | E-GEOD-44637 | biostudies-arrayexpress
Project description:CCCTC-binding factor (CTCF) is an architectural protein involved in the three-dimensional organization of chromatin. In this study, we systematically assayed the 3D genomic contact profiles of hundreds of CTCF binding sites in multiple tissues with high-resolution 4C-seq. We find both developmentally stable and dynamic chromatin loops. As recently reported, our data also suggest that chromatin loops preferentially form between CTCF binding sites oriented in a convergent manner. To directly test this, we used CRISPR-Cas9 genome editing to delete core CTCF binding sites in three loci, including the CTCF site in the Sox2 super-enhancer. In all instances, CTCF and cohesin recruitment were lost, and chromatin loops with distal CTCF sites were disrupted or destabilized. Re-insertion of oppositely oriented CTCF recognition sequences restored CTCF and cohesin recruitment, but did not re-establish chromatin loops. We conclude that CTCF binding polarity plays a functional role in the formation of higher order chromatin structure. 4C-seq was performed on a large number of viewpoints in E14 embryonic stem cells, neural precursor cells and primary fetal liver cells
2015-10-29 | E-GEOD-72539 | biostudies-arrayexpress
Project description:To identify genome-wide CCCTC binding factor (CTCF)-binding in A549 (ATCC CCL-185) and U2OS cells stably expressing rat GR (Rogatsky et al. , Mol Cell Biol, 1997. 17(6): p. 3181-93.) we performed ChIP-seq experiments upon hormone treatment (1.5 h, 1 M dexamethasone).
2018-04-12 | E-MTAB-5352 | biostudies-arrayexpress
Project description:The mammalian CCCTC-binding factor (CTCF) regulates gene expression through the formation of higher order chromatin structures. Recent evidence has implicated a role for CTCF in regulating gene expression in the human MHCII locus. To investigate the role of CTCF in murine MHCII gene expression we mapped CTCF binding sites in B cells (MHCII+ cells) and Plasmablasts which are differentiated B cells that have silenced MHCII gene expression. These observations lead to the identification of differential CTCF binding during differentiation in these cell types and suggest mechanims of MHCII gene regulation.
2014-02-05 | GSE44637 | GEO
Project description:We explored the microevolutionary trends of CTCF binding evolution by preforming ChIP-seq experiments in five closely related Mus strains, subspecies and species: Mus musculus domesticus, Mus musculus castaneus, Mus spretus, Mus caroli and Mus pahari. All experiments were performed in adult male liver samples in 3 biological replicates and with an input control set. Complementary RNA-seq data from this same study have been deposited in ArrayExpress under accession numebr E-MTAB-5768 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-5768 ).
2018-03-06 | E-MTAB-5769 | biostudies-arrayexpress
Project description:Chromosome segregation in mitosis and meiosis depends on sister chromatid cohesion mediated by cohesin complexes. Mutation of cohesin and other cohesion proteins causes transcriptional and developmental defects in animals and humans, but the molecular cause of these phenotypes is unknown. Here we describe 8811 cohesin binding sites in the human genome and show that the CCCTC-binding factor (CTCF) is associated with 88% of these. CTCF is dispensable for loading of cohesin onto DNA but is required for enrichment of cohesin at its binding sites. We provide evidence that cohesin is required for the role of CTCF sites in insulating promoters from distant enhancers. Like CTCF, cohesin is located on the maternal but not on the paternal allele of the H19 imprinting control region (ICR) and is required for imprinting of the H19-Igf2 locus. We find that cohesin is widely expressed in mammalian tissues, consistent with a cohesionindependent role in regulating gene expression. We propose that cohesin functions as a transcriptional insulator and speculate that subtle deficiencies in this function may be the cause of "cohesinopathies" such as Cornelia de Lange and Roberts syndrome. Keywords: ChIP-chip analysis
2008-01-30 | GSE9613 | GEO
Project description:CCCTC-binding factor (CTCF) is a conserved zinc finger transcription factor involved in chromatin looping. Recent evidence has shown a role for CTCF in ER biology. This experiment maps CTCF binding genome-wide in breast cancer cells and shows that CTCF binding does not change with estrogen or tamoxifen treatment. We find a small but reproducible proportion of CTCF binding events that overlap with both the nuclear receptor estrogen receptor and the forkhead protein FoxA1. These overlapping binding events are likely to be functional as they are biased towards estrogen-regulated genes. In addition, we identify cell-line specific CTCF binding events. These cell-line specific CTCF binding events are more likely to be associated with cell-line specific ER vinding events and are also more likely to be adjacent to genes that are expressed in that particular cell line. These data suggest a positive, pro-transcriptional role for CTCF in ER-mediated gene expression in breast cancer cells.
2011-12-07 | E-MTAB-740 | biostudies-arrayexpress