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Expression profiles of EDTA-dissociated colon epithelial cells of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice.

ABSTRACT: To assess potential changes in Wnt signaling more comprehensively, EDTA-dissociated colon epithelial cells from three pools of wild-type and Bcl9/Bcl9l-mutant mice were subjected to an exploratory comparative gene expression profiling.

ORGANISM(S): Mus musculus

PROVIDER: GSE21549 | GEO | 2010/09/01

SECONDARY ACCESSION(S): PRJNA129513

REPOSITORIES: GEO

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Expression profiles of EDTA-dissociated colon epithelial cells of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice.

Project description:To assess potential changes in Wnt signaling more comprehensively, EDTA-dissociated colon epithelial cells from three pools of wild-type and Bcl9/Bcl9l-mutant mice were subjected to an exploratory comparative gene expression profiling. Total RNA of three samples of EDTA-dissociated colon epithelial cells of wild-type mice and three samples of vil-Cre-Bcl9-/-/Bcl9l-/- mice, each sample consisting of material of two or three different mice, was collected and resulting amplified cDNA hybridized to Affymetrix Mouse Genome 430 2.0 arrays. Samples are labeled as follows: Genotype_PoolID _UniqueID_NumberOfMice.

2010-09-01 | E-GEOD-21549 | biostudies-arrayexpress

Expression profiles of colon epithelial cells and tumor samples of wild-type and vil-Cre-Bcl9-/-/Bcl9l-/- mice

Project description:This SuperSeries is composed of the following subset Series: GSE21549: Expression profiles of EDTA-dissociated colon epithelial cells of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice. GSE21576: Expression profiles of laser dissected colon tumor samples of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice Refer to individual Series

2010-09-01 | E-GEOD-21603 | biostudies-arrayexpress

Expression profiles of laser dissected colon tumor samples of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice

Project description:To investigate the impact of ablating Bcl9/Bcl9l on tumorigenesis, 6-8- week-old mice were exposed first to a single dose dimethylhydrazine (DMH, 44 mg/kg body weight), which is metabolized in the liver to carcinogenic azoxymethane (AOM), followed by 7 days oral administration of 2 % dextrane sulfate sodium (DSS) in the drinking water. This regimen results in the emergence of dysplastic adenomas, which progress to differentiated adenocarcinomas that are morphologically similar to human colorectal adenocarcinomas and typically harbor β-catenin stabilizing mutations of GSK3ß phosphorylation sites. Accordingly, these tumors present hallmarks of active Wnt signaling such as accumulation of nuclear β-catenin and expression of Wnt target genes. Total RNA of laser dissected samples from five different tumors each of two wild-type mice and three vil-Cre-Bcl9-/-/Bcl9l-/- mice was collected and resulting amplified cDNA hybridized to Affymetrix Mouse Genome 430 2.0 arrays. Samples are labeled as follows: Genotype_TumorID_MouseID_UniqueID.

2010-09-01 | E-GEOD-21576 | biostudies-arrayexpress

Expression profiles of laser dissected colon tumor samples of wild-type mice and vil-Cre-Bcl9-/-/Bcl9l-/- mice

2010-09-01 | GSE21576 | GEO

Mouse ameloblasts Bcl9 interactors

Project description:Bcl9 and Bcl9l (Bcl9l) are commonly thought as beta-catenin-dependent Wnt signaling transcriptional activators. We find however that, in the enamel-producin ameloblasts cells, Bcl9/9l are localiyed in the cytoplasm toward to apical secretory membrane. We performed pull down followed by mass spectrometry analysis to discover the molecular partners of Bcl9 that could explain this cytoplasmic localyzation.

2017-02-13 | PXD005449 | Pride

The specific interactions of Bcl9/Bcl9L with b-catenin and Pygopus promote breast cancer growth, invasion and metastasis

Project description:Summary: We studied how the binding of beta-catenin to the transcriptional coactivators B-cell CLL/lymphoma 9 (Bcl9) and Bcl9-Like (Bcl9L) affected mammary gland carcinogenesis in the MMTV-PyMT transgenic mouse model of metastatic breast cancer. Conditional knockout of both Bcl9 and Bcl9L resulted into tumor cell death. In contrast, disrupting the interaction of Bcl9/Bcl9L with beta-catenin, either by deletion of their HD2 domains or by a point mutation in the N-terminal domain of beta-catenin (D164A), diminished primary tumor growth and tumor cell proliferation and reduced tumor cell invasion and lung metastasis. In comparison, the effect of disrupting the HD1 domain-mediated binding of Bcl9/Bcl9L to Pygopus was more moderate. Interfering with the beta-catenin - Bcl9/Bcl9L - Pygo chain of adaptors only partially impaired the transcriptional response of mammary tumor cells to Wnt3a and TGF-beta treatment. The results indicate that Bcl9/Bcl9L critically enforce canonical Wnt signaling in its contribution to breast cancer growth and malignant progression.

2021-08-20 | GSE182404 | GEO

Pull down of full length and mutant BCL9 (deltaHD1) in mouse colorectal tumors and colonic epithelium

Project description:Bcl9 and Bcl9l (Bcl9l) are commonly thought as beta-catenin-dependent Wnt signaling transcriptional activators. Here we searched for BCL9 interacts that could explain the PYGO-independent phenotype induced be the loss of the HD1 (PYGO-binding) domain of BCL9

2020-08-10 | PXD018805 | Pride

RNA-seq experiment of developing mouse forelimbs, comparing Bcl9/9l mutant with control littermates.

Project description:Forelimbs were manually dissected from three individual Bcl9/9l-deltaHD1/deltaHD2 mutants and three control littermates, at 10.5 days post coitum. BCL9 and BCL9L are paralogous beta-catenin cofactors involved in the transcriptional machinery of Wnt target genes.

2020-05-08 | E-MTAB-9000 | biostudies-arrayexpress

Gene expression in DCIS.COM with BCL9 knockdown

Project description:There is limited research on which specific Wnt targets are regulated by B-Cell Lymphoma-9 (BCL9) and whether BCL9 regulates other signaling pathways to drive cancer malignancy. Here we demonstrated that BCL9 drives DCIS invasive progression by regulation of genes involved in cellular growth, invasion and migration.

2020-01-17 | GSE143790 | GEO

Targeted disruption of the BCL9/beta-catenin complex in cancer

Project description:Stabilized Alpha-Helix peptides of BCL9 HD2 (SAH-BCL9) block BCL9 and B9L interactions with beta-catenin and specifically downregulate Wnt target gene expression.

2012-08-23 | GSE33143 | GEO

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