SOX2 ChIP-Seq
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB43250 | ENA |
REPOSITORIES: ENA
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2014-12-15 | E-GEOD-58716 | biostudies-arrayexpress
Project description:Lineage-specific transcriptional regulators control differentiation states not only during normal development but also during cancer evolution. By investigating super-enhancer landscape of lung squamous cell carcinoma (LUSC), we identified a unique ‘neural’ subtype defined by Sox2 and a neural lineage factor Brn2. Robust protein-protein interaction and genomic co-occupancy of these factors indicated their transcriptional cooperation in this ‘neural’ LUSC in contrast to the cooperation of Sox2 and p63 in the classical LUSC. Introduction of p63 expression in the “neural’ LUSC invoked the classical LUSC lineage accompanied by Brn2 downregulation and increased activities of ErbB/Akt and MAPK-ERK pathways. Collectively, our data demonstrate a unique LUSC lineage featured by Sox2 cooperation with Brn2 instead of p63, for which distinct therapeutic approaches may be warranted.
2019-09-17 | GSE137459 | GEO
Project description:By integrating sequence information from closely related bacteria with a compendium of high-throughput gene expression datasets, a large-scale transcriptional regulatory networks was constructed for Rhodobacter sphaeroides. Predictions from this network were validated in part using genome-wide analysis for 3 transcription factors (PpsR, RSP_0489 and RSP_3341). Genome-wide protein-DNA interaction analysis of 3 transcription factors predicted to be involved in photosynthesis (PpsR), carbon metabolism (RSP_0489) and iron homeostasis (RSP_3341) were used to validate predictions from a large-scale reconstruction of R. sphaeroides transcriptional regulatory network.
2014-07-01 | E-GEOD-58648 | biostudies-arrayexpress
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.
2023-07-24 | GSE234703 | GEO
Project description:The control of cell identity is orchestrated by transcriptional and chromatin regulators in the context of specific chromosome structures. With the recent isolation of human naive embryonic stem cells (ESCs) representative of the ground state of pluripotency, it is possible to deduce this regulatory landscape in one of the earliest stages of human development. Here we generate cohesin ChIA-PET chromatin interaction data in naive and primed human ESCs and use it to reconstruct and compare the 3D regulatory landscapes of these two stages of early human development. The results reveal shared and stage-specific regulatory landscapes of topological domains and their subdomains, which consist of CTCF-CTCF/cohesin loops and enhancer-promoter/cohesin loops. The enhancer-promoter loop data reveal that genes with key roles in pluripotency are nearly always regulated by one or more super-enhancers, and show that these genes tend to occur in insulated neighborhoods. Our results reveal the key features of the 3D regulatory landscape of early human cells that form the foundation for embryonic development. ChIP-seq data from naive and primed human embroynic stem cells.
2015-11-22 | E-GEOD-69646 | biostudies-arrayexpress
Project description:BACKGROUND: SOX2 is a key gene implicated in maintaining the stemness of embryonic and adult stem cells. SOX2 appears to re-activate in several human cancers including glioblastoma multiforme (GBM), however, the detailed response program of SOX2 in GBM has not yet been defined. RESULTS: We show that knockdown of the SOX2 gene in LN229 GBM cells reduces cell proliferation and colony formation. We then comprehensively characterize the SOX2 response program by an integrated analysis using several advanced genomic technologies including ChIP-seq, microarray profiling, and microRNA sequencing. Using ChIP-seq technology, we identified 4883 SOX2 binding regions in the GBM cancer genome. SOX2 binding regions contain the consensus sequence wwTGnwTw that occurred 3931 instances in 2312 SOX2 binding regions. Microarray analysis identified 489 genes whose expression altered in response to SOX2 knockdown. Interesting findings include that SOX2 regulates the expression of SOX family proteins SOX1 and SOX18, and that SOX2 down regulates BEX1 (brain expressed X-linked 1) and BEX2 (brain expressed X-linked 2), two genes with tumor suppressor activity in GBM. Using next generation sequencing, we identified 105 precursor microRNAs (corresponding to 95 mature miRNAs) regulated by SOX2, including down regulation of miR-143, -145, -253-5p and miR-452. We also show that miR-145 and SOX2 form a double negative feedback loop in GBM cells, potentially creating a bistable system in GBM cells. CONCLUSIONS: We present an integrated dataset of ChIP-seq, expression microarrays and microRNA sequencing representing the SOX2 response program in LN229 GBM cells. The insights gained from our integrated analysis further our understanding of the potential actions of SOX2 in carcinogenesis and serves as a useful resource for the research community.
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2011-11-06 | E-GEOD-30738 | biostudies-arrayexpress
Project description:Mouse WT129 ESCs and differentiated from them within 12 days glutamatergic neurons were used for the ChiP-seq experiment with an antibody against Sox2 protein. ES stands for mESCs, NP for neurons, inputs are provided for both cell types.
2020-05-21 | E-MTAB-8196 | biostudies-arrayexpress
Project description:We performed ChIP-Seq of H3K27ac in duplicate in both WT and KO mesenchymal stem cells to evaluate global transcriptional changes between the new cells. We identified putative transcription factor binding sites using GEM v1.1 in K27ac data as well as in p MicroRNAs (miRNAs) are small non-coding RNAs that regulates development and disease but induce only moderate repression of directs mRNA targets, suggesting that they coordinate with other modes ofs cellular regulation to effect large changes in gene expression. Ins this work we decouple direct effects of global miRNA loss froms transcriptional changes downstream in a pair of isogenic murines fibroblast cell lines with and without Dicer expression. Wes demonstrate how effects on direct miRNA targets are amplified bys transcription machinery through the construction of a network models that identifies specific transcription factors that cause changes ins mRNA expression upon Dicer loss. Through transcription factors over-expression, we delineate miRNA-mediated transcriptional programss and identify miRNA-mediated coherent and incoherent feed-forwards loops, suggesting a functional role of the interaction between miRNAss and transcription factors. In total, our results indicate thats miRNAs tightly control transcription factors within a denses interconnected network to modulate gene expression. The experiment was designed to mimic the previously captured ChIP-Seq with two replicates in both WT and KO MSCs
2015-12-15 | E-GEOD-61034 | biostudies-arrayexpress
Project description:We analyzed the genome-wide binding of Sox2 and POU factor partner factors, Oct4 in ESCs (using published datasets PMID:18692474 and GSM307137, GSM307154, GSM307155) and Brn2 in NPCs. We found that Sox2 and Oct4 co-occupied a large subset of promoters and enhancers in ESCs, but that Sox2 and Brn2 co-occupy predominantly enhancers. Further, we overexpressed Brn2 in differentiating ESCs and showed that ectopic Brn2 recruited Sox2 to NPC-specific targets, resulting in skewed differentiation towards the neural lineage. Examination of transcription factor binding in ESCs, NPCs, and differentiating ESCs by ChIP-Seq.
2013-02-20 | E-GEOD-35496 | biostudies-arrayexpress