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ChIP-seq experiment of the beta-catenin co-factor Bcl9 in developing forelimbs.

ABSTRACT: ChIP-seq experiment of the beta-catenin co-factor Bcl9 in developing forelimbs.

PROVIDER: PRJEB31167 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3148730.fastq.gz	Fastqsanger.gz
	ERR3148726.fastq.gz	Fastqsanger.gz
	ERR3148727.fastq.gz	Fastqsanger.gz
	ERR3148728.fastq.gz	Fastqsanger.gz
	ERR3148729.fastq.gz	Fastqsanger.gz

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Similar Datasets

ChIP-seq experiment of the beta-catenin co-factor Bcl9 in developing forelimbs.

Project description:We isolated ca. 500 forelimbs at 10 days post coitum, and performed ChIP-seq using anti-Bcl9 antibodies. Bcl9 is a beta-catenin transcriptional cofactor, therefore it allows the identification of binding sites of the canonical Wnt signalling-dependent transcriptional complex. This experiment allowed to define that, in this developmental context, Bcl9 acts as a beta-catenin dedicated partner. Moreover, it established a series of genome-wide Bcl9 (therefore Wnt/beta-catenin) tissue-specific target loci, thereby assessing the genetic relationship existing between Wnt signaling and other signalling cascades (e.g. the Bmp pathway).

2019-02-21 | E-MTAB-7652 | biostudies-arrayexpress

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

ChIP-seq experiment of the beta-catenin co-factor BCL9 and the T-box transcription factor TBX3 in developing mouse forelimbs.

Project description:About 500 forelimbs were isolated at 10.5 days post coitum, and ChIP-seq was performed using anti-BCL9 (Abcam, ab37305) and anti-TBX3 (Santacruz, sc17871) antibodies. BCL9 is a beta-catenin transcriptional cofactor involved in the transcriptional machinery of Wnt target genes. TBX3 is a transcription factor important in limb development. This experiment identified, in this developmental context, co-occupancy of BCL9 and TBX3 on a genome-wide scale, and at Wnt-related loci, suggesting co-operation between these transcription factors in Wnt-driven limb development (Zimmerli et al. in revision during spring 2020). The following files are available for this experiment: - Raw sequencing data (.fastq) - Genomic enrichment data in bedgraph format (.bdg) which can be used for visualization in a genome browser. - Annotated peak files (.txt) containing high confidence peaks with genomic annotation. NOTE: The raw data relative to the BCL9 ChIP were previously deposited under accession number E-MTAB-7652, and described in Salazar et al. 2019. For simplicity, and to allow easy retrieval, we add the raw data of the entire experiment (including also BCL9) along with the newly generated analyses.

2020-05-08 | E-MTAB-8997 | biostudies-arrayexpress

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

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

| PRJEB38051 | ENA

ChIP-seq experiment of the beta-catenin co-factor BCL9 and the T-box transcription factor TBX3 in developing mouse forelimbs.

Project description:ChIP-seq experiment of the beta-catenin co-factor BCL9 and the T-box transcription factor TBX3 in developing mouse forelimbs.

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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

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. RNA from triplicate SAH-BCL9B- and vehicle-treated DLD1 samples (10 µM each for 12 hours) was hybridized to Affymetrix Human U133 Plus 2.0 arrays to asses global gene expression changes.

2012-08-23 | E-GEOD-33143 | biostudies-arrayexpress

BCL9/9L-Î²-catenin Signaling is Associated With Poor Outcome in Colorectal Cancer

Project description:Canonical Wnt signaling output is mediated by Î²-catenin, which interacts with LEF/TCF transcription factors and recruits a general transcriptional activation complex to its C-terminus. Its N-terminus binds BCL9/9L proteins, which bind co-activators that in mammals contribute to fine-tuning the transcriptional output. We found that a BCL9/9L-dependent gene expression signature was strongly associated with patient outcome in colorectal cancer and that stem cell and mesenchymal genes determine its prognostic value. Abrogating BCL9/9L-Î²-catenin signaling in independent mouse colorectal cancer models resulted in virtual loss of these traits, and oncogenic intestinal organoids lacking BCL9/9L proteins proved no longer tumorigenic. Our findings suggest that the BCL9/9L arm of Wnt-Î²-catenin signaling sustains a stemness-to-differentiation equilibrium in colorectal cancer, which critically affects disease outcome. Mutational activation of the Wnt pathway is a key oncogenic event in colorectal cancer. Targeting the pathway downstream of activating mutations is challenging, and the therapeutic window is limited by intestinal toxicity. Contrasting with phenotypes caused by inactivating key Wnt pathway components, ablation of BCL9/9L proteins in adult mice indicated that they were dispensable for intestinal homeostasis, consistent with their role in tuning transcription. Cancer stem cells are increasingly recognized as responsible for tumor recurrence. The correlation between stemness traits in colorectal cancer models and BCL9/9L-Î²-catenin signaling suggests that high Wnt signaling output is required for their maintenance. Our findings suggest that pruning Wnt-Î²-catenin signaling might be well tolerated and prove sufficient for trimming stemness traits and improving disease outcome. Examination of Bcl9/9l-knockout versus wild-type transcriptome in murine AOM-DSS tumors, APC-Kras tumors and healthy colocyte extracts.

2015-11-08 | E-GEOD-60837 | biostudies-arrayexpress

BCL9/9L-β-catenin Signaling is Associated With Poor Outcome in Colorectal Cancer

Project description:Canonical Wnt signaling output is mediated by β-catenin, which interacts with LEF/TCF transcription factors and recruits a general transcriptional activation complex to its C-terminus. Its N-terminus binds BCL9/9L proteins, which bind co-activators that in mammals contribute to fine-tuning the transcriptional output. We found that a BCL9/9L-dependent gene expression signature was strongly associated with patient outcome in colorectal cancer and that stem cell and mesenchymal genes determine its prognostic value. Abrogating BCL9/9L-β-catenin signaling in independent mouse colorectal cancer models resulted in virtual loss of these traits, and oncogenic intestinal organoids lacking BCL9/9L proteins proved no longer tumorigenic. Our findings suggest that the BCL9/9L arm of Wnt-β-catenin signaling sustains a stemness-to-differentiation equilibrium in colorectal cancer, which critically affects disease outcome. Mutational activation of the Wnt pathway is a key oncogenic event in colorectal cancer. Targeting the pathway downstream of activating mutations is challenging, and the therapeutic window is limited by intestinal toxicity. Contrasting with phenotypes caused by inactivating key Wnt pathway components, ablation of BCL9/9L proteins in adult mice indicated that they were dispensable for intestinal homeostasis, consistent with their role in tuning transcription. Cancer stem cells are increasingly recognized as responsible for tumor recurrence. The correlation between stemness traits in colorectal cancer models and BCL9/9L-β-catenin signaling suggests that high Wnt signaling output is required for their maintenance. Our findings suggest that pruning Wnt-β-catenin signaling might be well tolerated and prove sufficient for trimming stemness traits and improving disease outcome.

2015-11-08 | GSE60837 | GEO

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

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