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ChIP-seq analysis reveals key target genes of TCF on HUVECs

ABSTRACT: ChIP-seq analysis reveals key target genes of TCF on HUVECs

PROVIDER: PRJNA953950 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24116306_1.fastq.gz	Fastqsanger.gz
	SRR24116306_2.fastq.gz	Fastqsanger.gz
	SRR24116307_1.fastq.gz	Fastqsanger.gz
	SRR24116307_2.fastq.gz	Fastqsanger.gz
	SRR24116308_1.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis reveals key target genes of TCF on HUVECs

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Expression data from WT DN3, TCF-1-deficient DN3 thymocytes, and T cell lymphomas in TCF-1-deficient animals.

Project description:TCF-1 is an HMG family transcription factor which is known to be critical for T cell development. We discovered that it has a unique role in suppressing malignant transformation of developing thymocytes at early stages. We identified ID2 and LEF-1 as key TCF-1 target genens in tumor suppression. We used microarrays to detect gene expression changes in WT and TCF-1 deficient DN3 thymocytes as well as T cell lymphoma cells developed in TCF-1 KO mice. DN3 thymocytes were directly sorted from WT or TCF-1 KO mice. T cell lymphoma blast cells were also sorted from TCF-1 KO mice that developed the disease. RNA was extracted and hybridized to GeneChip Mouse GENE 1.0 ST arrays (Affymetrix).

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Expression data from WT DN3, TCF-1-deficient DN3 thymocytes, and T cell lymphomas in TCF-1-deficient animals.

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Transcription profiling of pancreatic islets in wild type and Tcf-1 knock-out mice to identify target genes Tcf-1 that may be responsible of mediating beta cell growth

Project description:Mutations in several transcription factors lead to a subtype of type 2 diabetes called maturity-onset diabetes of the young (MODY), which are characterized by autosomal dominant inheritance, an early age of disease onset, and development of marked hyperglycemia with a progressive impairment in insulin secretion (Shih and Stoffel, 2002). The most frequent form of MODY is caused by mutations in the gene encoding hepatocyte nuclear factor-1a (HNF-1a, TCF1). Mutant mice with loss of Tcf1 function as well as transgenic mice expressing a naturally occurring dominant-negative form of human TCF1(P291fsinsC) in pancreatic beta cells develop progressive hyperglycemia due to impaired glucose-stimulated insulin secretion (Hagenfeldt-Johansson et al., 2001; Yamagata et al., 2002). Importantly, these mice exhibit a progressive reduction in beta cell number, proliferation rate, and pancreatic insulin content. These data indicate that Tcf-1 target genes are also required for maintenance of normal beta cell mass. In this study we sought to identify target genes of Tcf-1 that may be responsible of mediating beta cell growth by comparing gene expression profiles of Tcf-1 knock-out and wild-type littermates in isolated pancreatic islets.

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

Project description:The microarray gene expression analysis revealed that TCF-4 isoforms activate different downstream target genes in HCC. TCF-4J upregulated genes associated with Wnt/beta-catenin, Notch, and insulin/IGF-1/IRS1 signal transduction pathway. 1 HAK-1A HCC clone overexpressing TCF-4J, 1 HAK-1A HCC clone overexpressing TCF-4K

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Intrinsically disordered domain of transcription factor TCF-1 is required for T cell developmental fidelity

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Tcf-1 expression in murine thymus

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DNAJA1 KO on HUVECs with heat stress

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