Beta-catenin dependent gene expression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA489972 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene experssion was evaluated in the lungs of mice in which beta-catenin was stabilized or knocked out in the SCGB1A1 lineage. Gene expression was assayed on post-natal day 21
2018-09-09 | GSE119687 | GEO
Project description:Interventions: Case series:Nil
Primary outcome(s): Ecadherin, beta catenin, CDX - 2, SOX - 2
Study Design: Non randomized control
| 2692541 | ecrin-mdr-crc
Project description:To elucidate the comprehensive changes regulated by β-catenin/TCF-dependent signaling in liver cancer cells, we explored a global gene expression of HepG2 cells after knockdown of β-catenin.
2017-09-01 | GSE94858 | GEO
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
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.
2018-11-02 | E-MTAB-7029 | biostudies-arrayexpress
Project description:In nucleated cells, β-catenin, the key downstream effector of this pathway, is a dual function protein, regulating the coordination of gene transcription and cell–cell adhesion. The specific role of β-catenin in the anucleate platelet however remains elusive. Here, we performed a label-free quantitative proteomic analysis of β-catenin immunoprecipitates from human platelets identifying 9 co-immunoprecipitating proteins. GO biological pathway analysis revealed a significant enrichment of specific functional terms including 'cell adhesion', 'cell junction organization' and ‘adherens junction organization'. Our bioinformatics data suggests that human platelet β-catenin may be involved in facilitating cell adhesion and cell junctions. We found three proteins co-immunoprecipitating with β-catenin under both resting and activated conditions, four proteins under resting condition only and two proteins under activated condition only.
2018-07-05 | PXD008130 | Pride
Project description:Wnt signaling regulates metazoan development and homeostasis, in part by β-catenin dependent activation and repression of a large number of genes. However, Wnt signaling also regulates genes independent of β-catenin, genes that are less well characterized. In this study, using a pan-Wnt inhibitor we performed a comprehensive transcriptome analysis in a Wnt-addicted orthotopic cancer model to delineate the β-catenin-dependent and independent arms of Wnt signaling. We find that while a large percentage of Wnt-regulated genes are regulated by β-catenin, ten percent of these genes are regulated independent of β-catenin. Interestingly, a large proportion of these β-catenin independent genes are Wnt-repressed.
2026-01-23 | GSE291732 | GEO
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:β-catenin plays a vital role in various biological processes, such as body axis determination and cell differentiation, during embryonic development in metazoans. These β-catenin functions are thought to be exerted through complexes formed with various types of proteins. Although β-catenin complex proteins have been identified in several bilaterian models, little is known about the structural and functional properties of β-catenin complexes in the early metazoan evolutionary phases. In this study, we performed a comparative analysis of β-catenin sequences in nonbilaterian lineages that branched off early in metazoan evolution. We aslo carried out a transphyletic function experiments of β-catenin from non-bilaterian metazoans using developing Xenopus embryos, which included secondary axis induction in embryos and proteomic analysis of the β-catenin protein complex. Comparative functional analysis of nonbilaterian β-catenins also demonstrated sequence characteristics important for β-catenin function, and the deep origin and evolutionary conservation of the cadherin-catenin complex. Proteins coimmunoprecipitated with β-catenin included several proteins conserved across metazoans. These data provide a new insight into the conserved repertoire of β-catenin complexes.
2025-01-21 | PXD053223 | JPOST Repository
Project description:Notch activation is instrumental in the development of most T-cell acute lymphoblastic leukemia (T-ALL) cases, yet Notch mutations alone are not sufficient to recapitulate the full human disease in animal models. Using multiple in vivo and in vitro T-ALL models we here demonstrate that β-Catenin is essential for Notch-driven T-cell leukemic initiation. Transcriptome analyses of leukemic initiating cells revealed a switch in β-Catenin activity that was Notch-context dependent. Moreover, ChIP-seq coupled with RNA-Seq in human Notch-active T-ALL showed that leukemic β-Catenin was independent of canonical LEF/TCF partners, and instead depended on direct association with Notch or ZBTB33/Kaiso for gene activation. The functional relevance of this mechanism is exemplified by the MYC 3´enhancer that requires β-Catenin and Notch1 recruitment to induce MYC expression. Finally, we demonstrate that pharmacological inhibition of β-Catenin with PKF115-584 prevented and partially reverted leukemogenesis induced by active Notch1. These microarray data show the transcriptional activities of N1IC and β-Catenin in wild-type or leukemic initiating cell (LIC) contexts in E14.5 FL LSK cells.
2023-01-01 | GSE69154 | GEO