SNP effect on chromatin accessibility (Whole genome sequencing)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA693318 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:SNP effect on chromatin accessibility (ChIP-Seq)
| PRJNA820602 | ENA
Project description:SNP effect on chromatin accessibility (RNA-Seq)
| PRJNA819956 | ENA
Project description:SNP effect on chromatin accessibility (ATAC-Seq)
| PRJNA819991 | ENA
Project description:Mammalian genome encodes approximately 1,700 transcription factors (TFs), 1,300 out of which have sequence specific binding motifs. Transcription in mammalian cells is regulated by the recruitment of TFs to specific cis-regulatory elements. In spite of consistent efforts on the function of individual TF, the question still remains how TFs bind to DNA and form enhancer. Here, we try to solve this problem by investigating the relationship between TF binding pattern and chromatin accessibility (ATAC-Seq). We first systematically acquired ATAC-Seq dataset as well as matched RNA-Seq dataset from different mouse primary tissues. A comprehensive TF binding map was built for each tissue/cell type by genomic approaches.
2022-07-21 | GSE165136 | GEO
Project description:The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of CTCF globally reduces chromatin interactions but does not significantly alter transcription. Here we systematically integrated multi-omics data including ATAC-seq, RNA-seq, WGBS, Hi-C, Cut&Run, CRISPR-Cas9 survival dropout screening, time-solved deep proteomic and phosphoproteomic analyses in cells carrying auxin-induced degron at endogenous CTCF locus. Acute CTCF protein degradation markedly rewired genome-wide chromatin accessibility. Increased accessible chromatin regions were largely located adjacent to CTCF-binding sites at promoter regions and insulator sites and were associated with enhanced transcription of nearby genes. In addition, we used CTCF-associated multi-omics data to establish a combinatorial data analysis pipeline to discover CTCF co-regulatory partners in regulating downstream gene expression. We successfully identified 40 candidates, including multiple established partners (i.e., MYC) supported by all layers of evidence. Interestingly, many CTCF co-regulators (e.g., YY1, ZBTB7A) that have evident alterations of respective downstream gene expression do not show changes at their expression levels across the multi-omics measurements upon acute CTCF loss, highlighting the strength of our system to discover hidden co-regulatory partners associated with CTCF-mediated transcription. This study highlights CTCF loss rewires genome-wide chromatin accessibility, which plays a critical role in transcriptional regulation
2021-07-04 | PXD026484 | Pride
Project description:Effect of mithramycin on chromatin accessibility (ATAC-Seq)
| PRJNA693316 | ENA
Project description:Effect of mithramycin on chromatin accessibility (ChIP-Seq)
| PRJNA765332 | ENA
Project description:Effect of mithramycin on chromatin accessibility (RNA-Seq)
| PRJNA693319 | ENA
Project description:Mammalian genome encodes approximately 1,700 transcription factors (TFs), 1,300 out of which have sequence specific binding motifs. Transcription in mammalian cells is regulated by the recruitment of TFs to specific cis-regulatory elements. In spite of consistent efforts on the function of individual TF, the question still remains how TFs bind to DNA and form enhancer. Here, we try to solve this problem by investigating the relationship between TF binding pattern and chromatin accessibility (ATAC-Seq). We first systematically acquired ATAC-Seq dataset as well as matched RNA-Seq dataset from different mouse primary tissues. A comprehensive TF binding map was built for each tissue/cell type by genomic approaches.
2022-07-21 | GSE199516 | GEO
Project description:Mammalian genome encodes approximately 1,700 transcription factors (TFs), 1,300 out of which have sequence specific binding motifs. Transcription in mammalian cells is regulated by the recruitment of TFs to specific cis-regulatory elements. In spite of consistent efforts on the function of individual TF, the question still remains how TFs bind to DNA and form enhancer. Here, we try to solve this problem by investigating the relationship between TF binding pattern and chromatin accessibility (ATAC-Seq). We first systematically acquired ATAC-Seq dataset as well as matched RNA-Seq dataset from different mouse primary tissues. A comprehensive TF binding map was built for each tissue/cell type by genomic approaches.
2022-07-21 | GSE199430 | GEO