Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SOX transcription factors direct TCF-independent Wnt/beta-catenin transcription

ABSTRACT: SOX transcription factors direct TCF-independent Wnt/beta-catenin transcription

PROVIDER: PRJNA758047 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15622200_1.fastq.gz	Fastqsanger.gz
	SRR15622200_2.fastq.gz	Fastqsanger.gz
	SRR15622201_1.fastq.gz	Fastqsanger.gz
	SRR15622201_2.fastq.gz	Fastqsanger.gz
	SRR15622102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 360

Similar Datasets

SOX transcription factors direct TCF-independent Wnt/beta-catenin transcription

Project description:We report ChIP-Seq experiments to profile the genomic binding dynamics of ß-catenin, SOX17, SOX2 and TCF/LEF TFs in definitive endoderm and neuromesodermal progenitor cells and RNA-Seq/ATAC-Seq experiments for transcriptomic and chromatin profiling of these cell types.

2022-07-27 | GSE182842 | GEO

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

Project description:During canonical Wnt signalling the activity of nuclear beta-catenin is largely mediated by the TCF/LEF family of transcription factors. To challenge this view we used the CRISPR/Cas9 genome editing approach to generate HEK 293T cell clones simultaneously carrying loss-of-function alleles of all four TCF/LEF genes. Exploiting unbiased whole transcriptome sequencing studies, we found that a subset of beta-catenin transcriptional targets did not require TCF/LEF factors for their regulation. Consistent with this finding, we observed in a genome-wide analysis that beta-catenin occupied specific genomic regions in the absence of TCF/LEF. Finally, we revealed the existence of a transcriptional activity of beta-catenin that specifically appears when TCF/LEF factors are absent, and refer to this as beta-catenin-GHOST response. Collectively, this study uncovers a previously neglected modus operandi of beta-catenin that bypasses the TCF/LEF transcription factors.

2018-11-22 | E-MTAB-7028 | biostudies-arrayexpress

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

2018-11-02 | E-MTAB-7029 | biostudies-arrayexpress

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

Project description:TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

| PRJEB27857 | ENA

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

Project description:TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

| PRJEB27856 | ENA

SOX transcription factors direct TCF-independent WNT/β-catenin responsive transcription to govern cell fate in human pluripotent stem cells.

Project description:WNT/β-catenin signaling controls gene expression across biological contexts from development and stem cell homeostasis to diseases including cancer. How β-catenin is recruited to distinct enhancers to activate context-specific transcription is unclear, given that most WNT/ß-catenin-responsive transcription is thought to be mediated by TCF/LEF transcription factors (TFs). With time-resolved multi-omic analyses, we show that SOX TFs can direct lineage-specific WNT-responsive transcription during the differentiation of human pluripotent stem cells (hPSCs) into definitive endoderm and neuromesodermal progenitors. We demonstrate that SOX17 and SOX2 are required to recruit β-catenin to lineage-specific WNT-responsive enhancers, many of which are not occupied by TCFs. At TCF-independent enhancers, SOX TFs establish a permissive chromatin landscape and recruit a WNT-enhanceosome complex to activate SOX/ß-catenin-dependent transcription. Given that SOX TFs and the WNT pathway are critical for specification of most cell types, these results have broad mechanistic implications for the specificity of WNT responses across developmental and disease contexts.

| S-EPMC10123531 | biostudies-literature

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [shRNA]

Project description:Constitutive activation of Wnt/β-catenin signaling drives tumor initiation, maintenance, and metastasis in numerous preclinical models. Within the nucleus, β-catenin interacts with transcription factors of the TCF/LEF (T cell factor/lymphoid enhancer factor, TCFs) family. The transcriptional program mediated by these β-catenin/TCF interactions promotes cell proliferation, epithelial-mesenchymal transition (EMT), and a cancer stem-cell phenotype. COLO320DM is a human colorectal cancer line with an activated Wnt/ β-catenin pathway driven by an APC mutation. Here, we apply a doxycycline-inducible shRNA to knockdown (KD) CTNNB1 (encoding β-catenin) and study the impact on the global transcriptome of COLO320DM. We also design and express an shRNA-resistant rescue cDNA to rule out any potential off-target effect. The results reveal a global gene expression change upon CTNNB1-KD that is consistent with β-catenin’s role in serving as a signal hub downstream of the canonical Wnt pathway.

2025-10-21 | GSE216381 | GEO

Expression data from Thymocytes of WT, TCF-1-deficient and β-catenin transgenic mice

Project description:Both TCF-1 and its coactivator β-catenin are known to be required for supporting normal double positive (DP) thymocyte survival through upregulating Bcl-xL. However, the downstream factors mediating this effect remained unknown. We used microarray to compare the global expression difference among WT, TCF-1-deficient, and β-catenin transgenic thymocytes to search for the genes that are down-regulated and up-regulated in TCF-1-deficient and β-catenin transgenic thymocytes, respectively. We focus on the genes that are significantly down-regulated and up-regulated in TCF-1-deficient and β-catenin transgenic thymocytes, respectively, to select for those genes that are potential target genes of β-catenin/TCF-1 pathway. And then those genes are subject to IPA pathway analysis searching for genes that are involved in thymocyte development and cell death.

2011-08-31 | E-GEOD-31371 | biostudies-arrayexpress

Insights into carcinogenic mechanisms of colorectal carcinoma lacking β-catenin/TCF regulated transcription.

Project description:We sought to identify the carcinogenic mechanisms involved in RKO cell line with no evidence of activated β-catenin/TCF regulated transcription, by comparison its gene expression profile to that of group of colorectal cancer cell lines selected to be mismatch repair deficient similar to RKO and having activate Wnt signaling.

2016-12-31 | GSE58058 | GEO

RNA-seq study of a helicon peptide targeting β-Catenin/TCF transcription factor [in vitro]

Project description:Genetic and epigenetic alterations in the Wnt signaling pathway leading to constitutive activation of the driver oncogene β-catenin occur in at least 20% of all human cancers. Pharmacologic suppression of aberrant β-catenin transcriptional activity through direct targeting of its downstream effectors has proven elusive despite decades of effort. We developed conformationally hyperstabilized α-helical peptides – which we refer to as Helicons – that directly bind β-catenin with sub-nanomolar affinity and exhibit good cytosolic exposure. COLO320DM is a human colorectal cancer line with an activated Wnt/ β-catenin pathway driven by an APC mutation. Here, we characterize the global effects of Helicon treatment on COLO320DM cells in vitro by whole-transcriptome RNA sequencing. As expected, Helicon 4 treatment had both time- and dose-dependent effects on the COLO320DM transcriptional profile. In particular, the Hallmark Wnt/β-catenin gene set was significantly down-regulated as early as six-hour at 10uM. The result validates the on-target inhibition of β-catenin signaling through disruption of its interaction with TCF/LEF transcription factors by active Helicons. COLO320DM is a human colorectal cancer line with an activated Wnt/ β-catenin pathway driven by an APC mutation. Here, we characterized the global effects of Helicon treatment on COLO320DM cells in vitro by whole-transcriptome RNA sequencing. As expected, Helicon 4 treatment had both time- and dose-dependent effects on the COLO320DM transcriptional profile. In particular, the Hallmark Wnt/β-catenin gene set was significantly down-regulated in as early as six -hours at 10 μuM. The result validates the on-target inhibition of β-catenin signaling through disruption of its interaction with TCF/LEF transcription factors by active Helicons.

2025-10-21 | GSE216379 | GEO

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