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Homo sapiens

ABSTRACT: Chip-Seq analysis of Sox2 protein genome-wide DNA binding sites in glioma cancer cells

PROVIDER: PRJNA133145 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR065790.fastq.gz	Fastqsanger.gz
	SRR065791.fastq.gz	Fastqsanger.gz
	SRR065792.fastq.gz	Fastqsanger.gz

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An integrative analysis of the SOX2 response program in glioblastoma

Project description:This SuperSeries is composed of the following subset Series: GSE23795: Chip-Seq analysis of Sox2 protein genome-wide DNA binding sites in glioma cancer cells GSE23838: Genes regulated by Sox2 in glioma cancer cell line Refer to individual Series

2011-01-10 | E-GEOD-23839 | biostudies-arrayexpress

Chip-Seq analysis of Sox2 protein genome-wide DNA binding sites in glioma cancer cells

Project description:We report here our results of the genome wide target identification of SOX2 in GBM cells by ChIP-seq analysis. Identification of Sox2 DNA binding site in glioma cancer cells

2011-01-10 | E-GEOD-23795 | biostudies-arrayexpress

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Project description:Genome-wide maps of SOX2 binding sites in lung cancer cells

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Pioneer activity distinguishes activating from non-activating SOX2 binding sites

Project description:Genome-wide transcriptional activity involves the binding of many transcription factors to thousands of sites in the genome. Determining which sites are directly driving transcription remains a challenge. Here we use acute protein depletion of the pioneer transcription factor SOX2 to establish its functionality in maintaining chromatin accessibility. We show that thousands of accessible sites are lost within an hour of protein depletion, indicating rapid turnover of these sites in the absence of pioneer factors. To understand the relationship with transcription we performed nascent transcription analysis and found that open chromatin sites that are maintained by SOX2 are highly predictive of gene expression, in contrast to all other SOX2 binding sites. We use CRISPR-Cas9 genome editing in the Klf2 locus to functionally validate a predicted regulatory element. We conclude that the regulatory activity of SOX2 is exerted largely at sites where it maintains accessibility and that other binding sites are largely dispensable for gene regulation.

2023-10-24 | PXD043672 | Pride

Pioneer activity distinguishes activating from non-activating SOX2 binding sites [ChIP-Seq]

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ChIP-seq anlysis of Sox2, Tfap2c, and Cdx2 in trophoblast stem cells.

Project description:To understand the mechanism underlying the transcriptional regulation by Sox2, we analyzed genome-wide binding sites of Sox2, Tfap2c, and Cdx2 in trophoblast stem (TS) cells by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq).

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Genome-wide maps of SOX2 binding sites in lung cancer cells

Project description:Discovery of SOX2 binding sites in lung cancer cells by CHIPseq and validate the target genes in two lung cancer cells by CHIP-QPCR.

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Distinct p53 Genomic Binding Patterns in Normal and Cancer-derived Human Cells

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.

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Project description:To understand the mechanism underlying the versatility in transcriptional regulation by Sox2 and Esrrb, we compared genome-wide binding sites of Sox2 and Esrrb in embryonic stem (ES) cells and trophoblast stem (TS) cells by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq).

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Project description:Genome-wide mapping of protein–DNA interactions is essential for a full understanding of transcriptional regulation. A precise map of binding sites for transcription factors, core transcriptional machinery is vital for deciphering the gene regulatory networks that underlie various biological processes. Chromatin immunoprecipitation followed by sequencing (ChIP–seq) is a technique for genome-wide profiling of DNA-binding proteins. However, our conventional ChIP–seq occasionally gives wider peaks which might be due to overlapping binding sites of two or more transcription factors. Therefore, to improve the resolution of our conventional ChIP–seq which have DNA-protein footprint of ~100 bp, we decreased the size of DNA-protein footprint to ~ 50 bp by DNaseI digestion of whole cell extract (WCE).

2014-02-06 | GSE40664 | GEO

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