Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA234069 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sf1+ mouse adrenocortical cells vs. Wnt-responsive mouse adrenocortical cells
| PRJNA234273 | ENA
Project description:In order to investigate genes regulated by Wnt/Beta-catenin-signaling in immortalized mouse adrenocortical cells, we treated a pair of ATCL7 cell cultures, one with BIO, a small molecule mimicking Wnt/Beta-catenin-signaling, the other with a control treatment. We repeated this 3 additional times resulting in 4 pairs of samples. The Wnt/beta-catenin pathway is not basally active in ATCL7 cells, nor do these cells appear to contain any mutations in the Wnt/Beta-catenin pathway. ATCL7 cells were grown under standard conditions at 37°C in a humidified incubator containing 5% CO2. 250,000 ATCL7 cells per sample were treated with 0.5uM BIO (6-Bromoindirubin-3'-oxime) or 0.01% DMSO (v/v) for 24 hours, in DMEM:F12 growth media containing 100U/mL pencillin/streptomycin, 1X insulin-transferrin-selenium-X, 0.025% fetal bovine serum and 0.025% horse serum. Cells were harvested and RNA was extracted using an RNeasy Plus Mini Kit (Qiagen). Biotinylated cDNA were prepared according to the Ambion WT kit protocol from 250 ng total RNA (GeneAtlas™ WT Expression Kit User Manual P/N 702935 Rev. 3). We assayed the targets with Affymetrix Mouse Gene ST 1.1 strip arrays. We modeled the data using paired T-tests for each probe-set. We also supply a supplementary file holding the data and some statistical analysis, as well as probe-set annotation that we used at that time (users may wish to obtain new annotation though). We analyzed only 28944 probe-sets with category "main", "---", and "flmrna->unmapped" according to Affymetrix annotation.
2014-07-11 | GSE53971 | GEO
Project description:SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complexes displace nucleosomes to promote the access of transcription factors to enhancers and promoters. Despite the critical roles of SWI/SNF in animal development and tumorigenesis, how signaling pathways recruit SWI/SNF complexes to their target genes is unclear. Here, we demonstrate that target gene activation mediated by Beta-catenin, the essential transcriptional coactivator in the Wnt signal transduction pathway, requires ubiquitylation of the SWI/SNF component Brahma-related gene-1 (BRG1) by the E3 ubiquitin ligase Thyroid Hormone Receptor Interactor 12 (TRIP12). TRIP12 depletion in Drosophila, zebrafish, mouse organoids, and human cells attenuates Wnt signaling. Genetic epistasis experiments place TRIP12 activity downstream of the Beta-catenin destruction complex. TRIP12 interacts with and ubiquitylates BRG1, and BRG1 depletion blocks TRIP12-mediated Wnt pathway activation. TRIP12 promotes BRG1 binding to Beta-catenin in the presence of Wnt. Our findings support a model in which TRIP12 ubiquitylates BRG1 in the presence of Wnt and promotes its interaction with Beta-catenin, thereby bringing SWI/SNF to Wnt target genes. Our studies suggest a general mechanism by which cell signaling induces the interaction between BRG1 and pathway-specific transcription factors to recruit SWI/SNF complexes to their appropriate target genes.
2024-01-06 | MSV000093784 | MassIVE
Project description:The mechanism by which Wnt signaling, an essential pathway controlling development and disease, stabilizes beta-Catenin has been a subject of debate over the last three decades. Casein kinase 1alpha (CK1a) functions as a pivotal negative regulator of this signaling pathway, initiating the events that destabilize beta-Catenin. However, whether and how CK1a activity is regulated in Wnt-off and Wnt-on states remains poorly understood. We now show that CK1a activity requires its association with the alpha catalytic subunit of Protein phosphatase 2A (PPP2CA) on AXIN, the scaffold protein of the beta-Catenin destruction complex. Wnt stimulation induces the dissociation of PPP2CA from CK1a, resulting in CK1a autophosphorylation and its consequent inactivation. Moreover, autophosphorylated CK1a is enriched in a subset of colorectal cancers (CRC) harboring constitutive Wnt activation. Our findings identify a novel mechanism by which Wnt stimulation inactivates CK1a, filling a critical gap in our understanding of Wnt signaling, with relevance for CRC.
| MSV000095904 | MassIVE
Project description:Mouse sustained epiblast-like cells established by Wnt/beta-catenin signaling manifest distinct features of formative pluripotency
| PRJNA856446 | ENA
Project description:In order to investigate genes regulated by Wnt/Beta-catenin-signaling in immortalized mouse adrenocortical cells, we treated a pair of ATCL7 cell cultures, one with BIO, a small molecule mimicking Wnt/Beta-catenin-signaling, the other with a control treatment. We repeated this 3 additional times resulting in 4 pairs of samples. The Wnt/beta-catenin pathway is not basally active in ATCL7 cells, nor do these cells appear to contain any mutations in the Wnt/Beta-catenin pathway. ATCL7 cells were grown under standard conditions at 37°C in a humidified incubator containing 5% CO2. 250,000 ATCL7 cells per sample were treated with 0.5uM BIO (6-Bromoindirubin-3'-oxime) or 0.01% DMSO (v/v) for 24 hours, in DMEM:F12 growth media containing 100U/mL pencillin/streptomycin, 1X insulin-transferrin-selenium-X, 0.025% fetal bovine serum and 0.025% horse serum. Cells were harvested and RNA was extracted using an RNeasy Plus Mini Kit (Qiagen). Biotinylated cDNA were prepared according to the Ambion WT kit protocol from 250 ng total RNA (GeneAtlas™ WT Expression Kit User Manual P/N 702935 Rev. 3). We assayed the targets with Affymetrix Mouse Gene ST 1.1 strip arrays. We modeled the data using paired T-tests for each probe-set. We also supply a supplementary file holding the data and some statistical analysis, as well as probe-set annotation that we used at that time (users may wish to obtain new annotation though). We analyzed only 28944 probe-sets with category "main", "---", and "flmrna->unmapped" according to Affymetrix annotation. ATCL7 cells were grown under standard growth conditions at 37°C in a humidified incubator containing 5% CO2. 250,000 ATCL7 cells per sample were treated for 24 hours with 0.5uM BIO (6-Bromoindirubin-3'-oxime) or 0.01% DMSO (v/v) in growth media containing 100U/mL pencillin/streptomycin, 1X insulin-transferrin-selenium-X, 0.025% fetal bovine serum and 0.025% horse serum. Cells were harvested and RNA was extracted using an RNeasy Plus Mini Kit (Qiagen). Biotinylated cDNA were prepared according to the Ambion WT kit protocol from 250 ng total RNA (GeneAtlas™ WT Expression Kit User Manual P/N 702935 Rev. 3). We assayed the targets with Affymetrix Mouse Gene ST 1.1 strip arrays.
2014-07-11 | E-GEOD-53971 | biostudies-arrayexpress
Project description:Pigment Epithelium-Derived Factor (PEDF) Inhibits Wnt/β-catenin Signaling in the Liver
| PRJNA268520 | ENA
Project description:Aberrant activation of the Wnt/β-catenin signaling pathway is a hallmark of colorectal cancer (CRC). Here, we identify the deubiquitinating enzyme USP17 as a critical regulator of β-catenin stability in CRC. We demonstrate that USP17 directly interacts with and deubiquitinates β-catenin, preventing its degradation and enhancing its stability. CRISPR/Cas9-mediated knockout of USP17 in CRC-derived cell lines significantly reduced β-catenin levels and suppressed epithelial-mesenchymal transition (EMT), as evidenced by distinct morphological changes and altered expression of classical EMT markers. USP17 depletion reduced the proliferation of CRC cell lines and impaired CRC tumor growth in vivo. Conversely, USP17 overexpression in immortalized rat enterocytes elevated β-catenin levels and enhanced KRAS-induced cell proliferation. RNA sequencing and quantitative proteomic analysis of USP17-depleted CRC cells revealed significant suppression of the transcriptional coactivator function of β-catenin, impacting key oncogenic-related pathways. Our findings establish USP17 as a key regulator of β-catenin signaling and highlight its potential as a candidate therapeutic target in CRC.
2026-02-25 | PXD065117 | Pride
Project description:Nucleoredoxin is required for the maintenance of Wnt/β-catenin signaling in mice embryo
| PRJNA127245 | ENA
Project description:Investigate the role of Wnt/beta-catenin signaling in development of the exocrine pancreas
| PRJNA97951 | ENA