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RMST associates with SOX2 to regulate neurogenesis [Illumina expression data]

ABSTRACT: We report that knockdown of the lncRNA RMST changes the gene expression profile of neural stem cells. RMST and SOX2 regulates a common subset of downstream targets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE49403 | GEO | 2013/08/01

SECONDARY ACCESSION(S): PRJNA213906

REPOSITORIES: GEO

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RMST associates with SOX2 to regulate neurogenesis [Illumina expression data]

Project description:We report that knockdown of the lncRNA RMST changes the gene expression profile of neural stem cells. RMST and SOX2 regulates a common subset of downstream targets. Examination of genome wide transcriptomic changes upon knockdown of the lncRNA RMST.

2013-08-01 | E-GEOD-49403 | biostudies-arrayexpress

RMST associates with SOX2 to regulate neurogenesis [ChIP-Seq]

Project description:We report that knockdown of the lncRNA RMST changes the chromatin binding profile of the transcription factor SOX2. Examination of SOX2 chromatin binding profile under normal and RMST-depleted conditions in differentiating neural stem cells.

2013-08-01 | E-GEOD-49404 | biostudies-arrayexpress

RMST associates with SOX2 to regulate neurogenesis [ChIP-Seq]

Project description:We report that knockdown of the lncRNA RMST changes the chromatin binding profile of the transcription factor SOX2.

2013-08-01 | GSE49404 | GEO

RMST associates with SOX2 to regulate neurogenesis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-01 | E-GEOD-49405 | biostudies-arrayexpress

RMST associates with SOX2 to regulate neurogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-08-01 | GSE49405 | GEO

Identification the Expression of Sox2 in Colorectal Cancer Tissues

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

Competitive binding of E3 ligases TRIM26 and WWP2 controls SOX2 in glioblastoma

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

CUT&RUN Targeting c-FOS, c-JUN and SOX2 in neurospheres derived from mouse brain cells

Project description:Other than in the development of the brain, SOX2 is essential for the long-term self-renewal of neural stem cells (NSCs). The mechanisms of how SOX2 maintains the stemness of NSCs is not yet understood. We have identified Fos as a downstream target of SOX2, and therefore used CUT&RUN to investigate where these transcription factors - and the c-FOS partner c-JUN - interact with the genome. By comparing binding patterns of c-FOS, c-JUN and SOX2, we find that they co-occupate the promoter of the SOCS3 locus, which we also have identified as a gene that rescues SOX2 deletion induced senescence when overexpressed in neurospheres grown from Sox2-deleted mouse NSCs. Taken together, our data provide a basis for elucidating a gene regulatory network necessary for the maintenance of self-renewal in post-embryonic neural stem cells.

2021-04-01 | E-MTAB-9897 | biostudies-arrayexpress

Sox2 ChIPSeq

Project description:Sox2 and Chd7 ChIP seq data in neural stem cells

| PRJEB2184 | ENA

NANOG-OCT4-SOX2 Regulatory Module in Human Embryonic Stem Cells (dataset 1)

Project description:The transcription factors Nanog, Oct4 and Sox2 are the master regulators of pluripotency in mouse embryonic stem cells (mESCs), however, their functions in human ESCs (hESCs) have not been rigorously defined. Here we show that the requirements for NANOG, OCT4 and SOX2 in hESCs differ from those in mESCs. Both NANOG and OCT4 are required for self-renewal and repress differentiation. OCT4 controls both extraembryonic and epiblast-derived cell fates in a BMP4-dependent manner. OCT4-depleted hESCs commit to trophectoderm and primitive endoderm in the presence of BMP4, but undergo neuroectoderm differentiation in the absence of BMP4. NANOG represses neuroectoderm and neural crest commitment, but has little or no effect on the other lineages. We find that SOX2 is not required for self-renewal because it is redundant with SOX3, which is induced in SOX2-depleted hESCs. Simultaneous depletion of both SOX2 and SOX3 induces differentiation into the primitive streak. Unexpectedly, we identify significant variability in the usage of pluripotency factors by individual hESC lines, suggesting that the pluripotency network is remodelled to support a continuum of developmental states. Our study revises the general view of how NANOG, OCT4 and SOX2 orchestrate self-renewal in hESCs. Total RNA obtained from H1P (control)-, shNANOG (Nanog shRNA knockdown)-, shOCT4 (Oct4 shRNA knockdown)- or shSOX2 (Sox2 shRNA knockdown)-transduced hESCs for 8 days time course.

2012-04-05 | E-GEOD-34904 | biostudies-arrayexpress

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