Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18330504.fastq.gz | Fastqsanger.gz | |||
| SRR18330505.fastq.gz | Fastqsanger.gz | |||
| SRR18330506.fastq.gz | Fastqsanger.gz |
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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:Here we have developed a method to identify chromatin-bound partners of a protein of interest by selective isolation of chromatin-associated proteins (SICAP) followed by mass spectrometry. We applied SICAP to identify chromatin-binding proteins associated to Oct4, Sox2 and Nanog in mouse embryonic stem (ES) cells.
2016-12-19 | PXD003798 | Pride
Project description:A subset of transcription factors is proposed to form functional interactions with RNA to facilitate proper regulation of gene expression. Sox2, a critical transcription factor for maintenance of pluripotency and neurogenesis, is found associated with several lncRNAs, although it is unknown whether these interactions are direct or via other proteins. We demonstrate that human Sox2 interacts directly with one of these lncRNAs with high affinity through its HMG DNA-binding domain. Furthermore, rather than interacting with a single high affinity site, Sox2 binds regions of dsRNA in a non-sequence specific fashion. RNA binding is competitive with dsDNA, yet interaction with RNA is primarily electrostatically driven using a partially overlapping set of amino acids as that used for DNA binding. Finally, we use two distinct crosslinking techniques, formaldehyde and UV, with RNA immunoprecipitation (respectively, “fRIP” and “UVRIP”) of Sox2 in mouse embryonic stem cells to identify >1000 potential Sox2-RNA interacting partners with ~75% overlap between the two techniques. Together, these data reveal that Sox2 productively binds dsRNA with affinities rivaling ChIP-validated promoter DNA sites, suggesting that the transcriptome plays a significant role in regulation of gene expression by Sox2.
2020-03-16 | GSE142013 | GEO
Project description:Advances in molecular strategies to reprogram cell fate is a promising avenue for cell-based therapies. Methods to generate induced neural stem cells (iNSCs) are often slow with limited reprogramming events and it is unclear whether cells transit via a pluripotent state. We report an iNSC reprogramming approach from embryonic and aged mouse fibroblasts using an engineered Sox17 (eSox17FNV). eSox17FNV efficiently drives iNSC reprogramming while Sox2 or Sox17 fails to do so. eSox17FNV acquires the capacity to bind new protein partners to scan the genome more efficiently and possesses a more potent transactivation domain than Sox2. At the onset of reprogramming, in the presence of eSox17FNV, fibroblasts divert from a iPSC route towards iNSC fate. Further, lineage tracing shows that emerging iNSCs do not transit through a pluripotent state if POU factors are excluded. This reveals new molecular and physiological framework for iNSC generation and contrasts with lineage from pluripotency reprogramming.
2023-07-19 | GSE195554 | GEO
Project description:The pluripotency transcription factor SOX2 is essential for the maintenance of glioblastoma stem cells (GSC), which drive tumor growth and treatment resistance.To understand how SOX2 is regulated in GSCs, we utilized a proteomic approach and identified the E3 ubiquitin ligase TRIM26 as a direct SOX2-interacting protein. Unexpectedly, we found TRIM26 depletion decreased SOX2 protein levels and increased SOX2 polyubiquitination in patient-derived GSCs, suggesting TRIM26 promotes SOX2 protein stability. Accordingly, TRIM26 knockdown reduced SOX2 transcriptional activity, self-renewal capacity, and in vivo tumorigenicity in multiple GSC lines. Mechanistically, we found TRIM26, via its C-terminal PRYSPRY domain, but independent of its RING domain, stabilizes SOX2 protein by directly inhibiting the interaction of SOX2 with WWP2, which we identify as a bona fide SOX2 E3 ligase in GSCs. Our work identifies E3 ligase competition as a critical mechanism of SOX2 regulation, with functional consequences for GSC identity and maintenance.
2021-11-04 | PXD028933 | Pride
Project description:Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: Sox2 ChIP-enriched DNA and input DNA was isolated from gastric glands of adult antrum from Sox2 KO and Sox2 WT mice. DNA was purified and genomic libraries were prepared as described (Sulahian et al., 2014), using four micrograms of goat anti-SOX2 (AF2018, R&D). Libraries were sequenced (50 bp, single-end reads) on an Illumina Hi-Seq 2000 instrument. Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of wnt, intestinal and cancer related genes Examination of Sox2 targets in the stomachs of Sox2 WT and Sox2 KO mice.
2016-08-04 | E-GEOD-83965 | biostudies-arrayexpress
Project description:SOX2 is a transcription factor essential for pluripotent stem cells, and development and maintenance of squamous epithelium. We previously reported SOX2 an oncogene subject to highly recurrent genomic amplification in squamous cell carcinomas (SCCs). Here we demonstrate in SCCs that SOX2 interacts with another master squamous transcription factor p63, and through ChIP-seq show that genomic occupancy of SOX2 overlaps with that of p63 at a large number of loci and that they cooperatively regulate gene expression including ETV4, which we find essential for SOX2-amplified SCC cell survival. Furthermore, SOX2 binds to distinct genomic loci in SCCs than in embryonic stem cells and the SOX2-p63 coordinate binding is unique to SCC. In addition, a subset of SOX2 genomic binding sites in SCC that lack p63 co-occupancy are co-occupied by the AP-1 transcriptional complex. These demonstrate that SOX2’s actions in SCC differ substantially from its role in pluripotency and identify novel SOX2 interactions that will enable deeper characterization of SOX2’s function in SCC. SOX2 and p63 ChIP-seq from three lung and esophageal squamous carcinoma cell lines with amplification of SOX2 as well as SOX2 ChIP-seq from an ES cells.
2014-03-12 | E-GEOD-46837 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE29179: Identification of differentially expressed genes upon shRNA knockdown of TAL1 and its regulatory partners in T-ALL cells (Jurkat) GSE29180: ChIP-Seq of TAL1 and its regulatory partners in T-ALL cells (Jurkat) GSE33850: Core transcriptional regulatory circuit controlled by the tal1 complex in human t-cell acute lymphoblastic leukemia (Subseries) Refer to individual Series
2012-08-16 | E-GEOD-29181 | biostudies-arrayexpress
Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes.
2013-05-22 | GSE45427 | GEO