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Tcf ChIP_Seq analysis in cultured differentiated TSC cells at the presence of DMSO or CHIRGene expression in the placenta of WT and Ctnnb1 overexpression mice

ABSTRACT: Tcf ChIP_Seq analysis in cultured differentiated TSC cells at the presence of DMSO or CHIRGene expression in the placenta of WT and Ctnnb1 overexpression mice

PROVIDER: PRJNA610575 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11244977_1.fastq.gz	Fastqsanger.gz
	SRR11244977_2.fastq.gz	Fastqsanger.gz
	SRR11244978_1.fastq.gz	Fastqsanger.gz
	SRR11244978_2.fastq.gz	Fastqsanger.gz

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Tcf ChIP_Seq analysis in cultured differentiated TSC cells at the presence of DMSO or CHIRGene expression in the placenta of WT and Ctnnb1 overexpression mice

Project description:Wnt signaling are essential for the maintenance and differentiation of stem/progenitor cells, including trophoblast stem cells during placental development. Hyper-activation of Wnt signaling has been shown to relate with human trophoblast diseases. However, litter is known about the impact and underlying mechanisms of excessive Wnt signaling during placental trophoblast development. In the present work, we found that Sfrp1,5 double mutant mouse exhibited disturbed trophoblast differentiation in the placental ectoplacental cone (EPC), where the precursors of secondary trophoblast giant cells (TGCs) and trophoblast cells in the spongiotrophoblast layer are located. Employing mouse models expressing a trunked β-catenin with exon 3 deletion globally and trophoblast-specifically, combining cultured trophoblast stem cells, we found that hyper-activation of canonical Wnt pathway exhausted the trophoblast precursor cells in the EPC, resulting in the overabundance of giant cells at the expense of spongiotrophoblast cells. Further examination uncovered that hyper-activation of canonical Wnt pathway disturbed trophoblast differentiation in the EPC via repressing Mash2 expression. Collectively, our findings demonstrate that appropriate canonical Wnt-β-catenin pathway is essential for EPC trophoblast differentiation during placental development. Our work also has high clinical relevance, since abnormal Wnt signaling are often associated with trophoblast-related diseases.

2020-03-06 | GSE146432 | GEO

ChIP_seq

Project description:ChIP_seq

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Expression data from human adrenocortical H295R cells expressing a doxycyclin-inducible shRNA targeting CTNNB1

Project description:We used the H295R cell line, human adrenocortical cells, harboring a heterozygous CTNNB1 (beta-catenin) gene mutation affecting the GSK3 beta-phosphorylation site (S45P) and leading to constitutive transcriptional activity of beta-catenin-LEF/TCF. Whole-transcript gene expression was analyzed in three stable clones of H295R cells expressing a doxycycline-inducible shRNA targeting CTNNB1 mRNA and in a control clone, without or with doxycycline for 5 days.

2015-08-03 | E-MTAB-3330 | biostudies-arrayexpress

CTNNB1 mutations and overexpression of Wnt/beta-catenin target genes in WT1-mutant Wilms' tumors

Project description:Gain-of-function mutations in exon 3 of beta-catenin (CTNNB1) are specific for Wilms' tumors that have lost WT1, but 50% of WT1-mutant cases lack such "hot spot" mutations. To ask whether stabilization of beta-catenin might be essential after WT1 loss, and to identify downstream target genes, we compared expression profiles in WT1-mutant versus WT1 wild-type Wilms' tumors. Supervised and nonsupervised hierarchical clustering of the expression data separated these two classes of Wilms' tumor. The WT1-mutant tumors overexpressed genes encoding myogenic and other transcription factors (MOX2, LBX1, SIM2), signaling molecules (TGFB2, FST, BMP2A), extracellular Wnt inhibitors (WIF1, SFRP4), and known beta-catenin/TCF targets (FST, CSPG2, CMYC). Beta-Catenin/TCF target genes were overexpressed in the WT1-mutant tumors even in the absence of CTNNB1 exon 3 mutations, and complete sequencing revealed gain-of-function mutations elsewhere in the CTNNB1 gene in some of these tumors, increasing the overall mutation frequency to 75%. Lastly, we identified and validated a novel direct beta-catenin target gene, GAD1, among the WT1-mutant signature genes. These data highlight two molecular classes of Wilms' tumor, and indicate strong selection for stabilization of beta-catenin in the WT1-mutant class. Beta-Catenin stabilization can initiate tumorigenesis in other systems, and this mechanism is likely critical in tumor formation after loss of WT1. Keywords: single channel

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ChIP_Seq analysis in cultured hTSCs

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Peg10 regulation of TSC differentiation

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Spatial transcriptomics of TSC angiomyolipoma

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Tcf-1 expression in murine thymus

Project description:The DNA binding factor Tcf-1 is one of the most prominently expressed genes in thymocytes yet it's global DNA binding pattern remained unknown. Here we have assessed by ChIP-seq the Tcf-1 binding pattern in murine thymocytes. Tcf-1 ChIP-seq of 1 sample and input control.

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Human HAK-1A hepatocellular carcinoma (HCC) cells: TCF-4J-overexpressing clone (under normoxia) vs. TCF-4K-overexpressing clone (under normoxia)

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2013-11-01 | E-GEOD-42512 | biostudies-arrayexpress

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