Similar Datasets
Project description:Sox2 has been studied in several types of human solid tumors. The investigators found that Sox2 had higher expression level in colorectal cancer and metastatic tissues than normal tissues. So the investigators assumed that whether Sox2 plays an important role in the progression and migration of colon cancer.
| 2124687 | ecrin-mdr-crc
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
Project description:4C-seq was performed to assess genomic contacts with the SOX2 protmoter, human neural stem cells with no oncogenic alterations were compared to those with concurrent IDH1-R132H overexpression, P53 shRNA knockdown and ATRX shRNA knockdown.
2017-11-09 | GSE94961 | GEO
Project description:Sox2 is a key transcription factor directing embryonic stem cell (ESC) pluripotency. However, the role of SoxB1 proteins in epiblast stem cell (EpiSC) pluripotency is unknown. Here we compare the transcriptomes of pluripotent cells cultured in different conditions that express different levels of Sox2. While highest Sox2 level in ESCs are enriched for naive pluripotency markers, ESCs and EpiSCs expressing the same Sox2 level were transcriptionally distinct. Thus Sox2 levels do not dictate the distinction between ESC and EpiSC states.
2017-12-19 | GSE99185 | GEO
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.
2013-02-20 | GSE35496 | GEO
Project description:Cellular differentiation requires cells to undergo dramatic but strictly controlled changes in chromatin organization, transcriptional regulation, and protein production and interaction. To understand the regulatory connections between these processes, we applied a multi-omics approach integrating proteomic, transcriptomic, chromatin accessibility, protein occupancy, and protein-chromatin interaction data acquired during differentiation of mouse embryonic stem cells (ESCs) into post-mitotic neurons. We found extensive remodeling of the chromatin that was preceding changes on RNA and protein levels. We found the pluripotency factor Sox2 as regulator of neuron-specific genes and, as a potential mechanism, revealed its genomic redistribution from pluripotency enhancers to neuronal promoters and concomitant change of its protein interaction network upon differentiation. We identified Atrx as a major Sox2 partner in neurons, whose co-localisation correlated with an increase in active enhancer marks and increased expression of nearby genes, and where deletion of a Sox2-Atrx co-bound site resulted in reduced expression of the proximal gene. Collectively, these findings provide key insights into the regulatory transformation of Sox2 during neuronal differentiation and highlight the significance of multi-omic approaches in understanding gene regulation in complex systems.
2020-06-04 | PXD016080 | Pride
Project description:Embryonic stem cell (ESCs) identity is orchestrated by co-operativity between the transcription factors (TFs) Sox2 and the class V POU-TF, Oct4 at composite Sox/Oct motifs. Neural stem cells (NSCs) lack Oct4 but express Sox2 and class III POU-TFs. This raises the question of how Sox2 interacts with POU-TFs to transcriptionally specify ESCs or NSCs. Here we show that Oct4 alone binds the Sox/Oct motif and the octamer-containing palindromic MORE equally well. Sox2 binding selectively increases the affinity of Oct4 for the Sox/Oct motif. In contrast, Oct6 binds preferentially to the MORE, and is unaffected by Sox2. ChIP-seq in NSCs shows the MORE to be the most enriched motif for class III POU-TFs, with MORE sub-types apparent, but no Sox/Oct motif enrichment. These results suggest that in NSCs, co-operativity between Sox2 and class III POU-TFs may not occur and that POU-TF driven transcription uses predominantly the MORE cis architecture. Thus, distinct interactions between Sox2 and POU-TF subclasses distinguish pluripotent ESCs from multipotent NSCs, providing molecular insight into how Oct4 alone can convert NSCs to pluripotency.
2015-08-21 | GSE69859 | GEO
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:The pluripotency of embryonic stem cells (ESCs) is maintained by a small group of master transcription factors including Oct4, Sox2 and Nanog. These core factors form a regulatory circuit controlling the transcription of a number of pluripotency factors including themselves. Although a lot of previous studies have identified key factors regulating this core network in trans, the contribution of cis-regulatory DNA sequences on the transcription of these key pluripotency factors remains elusive. We analyzed epigenomic data within the 1.5 Mb gene-desert regions around Sox2 gene and predicted only one 13kb-long enhancer located 100kb downstream of Sox2 in mouse ES cells. This enhancer is occupied by Oct4, Sox2, Nanog, and mediator complex and forms a long-range DNA looping to Sox2 locus. We hypothesized that this enhancer is critical for Sox2 gene expression and tested this hypothesis by deleting this entire 13-kb enhancer with a simple highly-efficient double-excision CRISPR strategy. Allele-specific of Sox2 transcripts in heterozygous enhancer-deletion clones showed that the enhancer affects expression through a cis-acting mechanism. Strikingly, although this distal enhancer is not conserved in other mammals including human, it is responsible for over 90% of Sox2 expression in mouse ESCs. Taken together, our results provide direct evidence that in mouse ESCs, Sox2 transcription is primarily driven by a species-specific distal enhancer, which may provide new perspectives explaining the physiological difference between human and mouse ES cells. This dataset include ChIP-seq of H3K4me3 and H3K27ac in a hybrid mouse ES cells (F123). H3K27ac in J1 mouse ES cells. And RNA-seq in F123 mESCs with complete Sox2 enhancer deletion or enhancer haploinsufficient clones.
2014-12-09 | E-GEOD-60763 | biostudies-arrayexpress