Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ribo-seq of human breast cancer cell line MCF7 overexpressing different full length SOX2, N-terminal SOX2 and C-terminal SOX2 with nuclear export signal

ABSTRACT: Ribo-seq of human breast cancer cell line MCF7 overexpressing different full length SOX2, N-terminal SOX2 and C-terminal SOX2 with nuclear export signal

PROVIDER: PRJEB63358 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR11583300.fastq.gz	Fastqsanger.gz
	ERR11583301.fastq.gz	Fastqsanger.gz
	ERR11583302.fastq.gz	Fastqsanger.gz
	ERR11583303.fastq.gz	Fastqsanger.gz
	ERR11583304.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

RNA-seq of human breast cancer cell line MCF7 overexpressing different full length SOX2, N-terminal SOX2 and C-terminal SOX2 with nuclear export signal

Project description:RNA-seq of human breast cancer cell line MCF7 overexpressing different full length SOX2, N-terminal SOX2 and C-terminal SOX2 with nuclear export signal

| PRJEB63355 | ENA

Ribo-seq of human breast cancer cell line MCF7 overexpressing different full length SOX2, N-terminal SOX2 and C-terminal SOX2 with nuclear export signal

Project description:Understanding the role of transcription factor SOX2 in translational control in breast cancer.

2025-01-01 | E-MTAB-13099 | biostudies-arrayexpress

RNA-seq of human breast cancer cell line MCF7 overexpressing different full length SOX2, N-terminal SOX2 and C-terminal SOX2 with nuclear export signal

Project description:Understanding the role of transcription factor SOX2 in translational control in breast cancer.

2024-01-01 | E-MTAB-13098 | biostudies-arrayexpress

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation [ChIP-seq]

Project description:The histone 3 lysine 9 (H3K9)-specific methyltransferase (KMT) Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 role(s) in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for muscle adult stem cells expansion following activation and in vitro studies on skeletal myoblasts confirmed that Setdb1 suppresses terminal myoblast differentiation. We used genome-wide analyses to identify Setdb1 direct target genes in myoblasts and observed a release of Setdb1 from the promoter of selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. We demonstrated that both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Taken together, our findings uncover a functional link between Setdb1 and canonical Wnt signalling in skeletal muscle cells, which affects the expression of a subset of Setdb1 target genes. We revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions. ChIP-seq of Setdb1 and H3K9me3 in Myoblast cells (C2C12)

2016-02-01 | E-GEOD-65493 | biostudies-arrayexpress

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation

Project description:The histone 3 lysine 9 methyltransferase Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 roles in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for adult muscle stem cells expansion following activation. In vitro studies in skeletal myoblasts confirmed that Setdb1 suppresses terminal differentiation. Genomic binding analyses showed a release of Setdb1 from selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. Both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Transcriptomic assays in myoblasts unravelled a significant overlap between Setdb1 and Wnt3a regulated genetic programs. Together, our findings revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions and myogenesis. This SuperSeries is composed of the SubSeries listed below.

2016-02-01 | GSE70070 | GEO

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation [RNA-seq]

Project description:The histone 3 lysine 9 methyltransferase Setdb1 is essential for both stem cell pluripotency and terminal differentiation of different cell types. To shed light on Setdb1 roles in these mutually exclusive processes, we used mouse skeletal myoblasts as a model of terminal differentiation. Ex vivo studies on isolated single myofibres showed that Setdb1 is required for muscle adult stem cells expansion following activation. In vitro studies in skeletal myoblasts confirmed that Setdb1 suppresses terminal myoblast differentiation. Genomic binding analyses showed a release of Setdb1 from the promoter of selected target genes upon myoblast terminal differentiation, concomitant to a nuclear export of Setdb1 to the cytoplasm. Both genomic release and cytoplasmic Setdb1 relocalisation during differentiation were dependent on canonical Wnt signalling. Together, our findings revealed Wnt-dependent subcellular relocalisation of Setdb1 as a novel mechanism regulating Setdb1 functions and adult myogenesis.

2016-02-01 | GSE70069 | 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

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation

Project description:Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation

| PRJNA287564 | ENA

Canonical Wnt signalling regulates nuclear export of Setdb1 during skeletal muscle terminal differentiation [ChIP-seq]

2016-02-01 | GSE65493 | GEO

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data