Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA145897 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Both TCF-1 and its coactivator β-catenin are known to be required for supporting normal double positive (DP) thymocyte survival through upregulating Bcl-xL. However, the downstream factors mediating this effect remained unknown. We used microarray to compare the global expression difference among WT, TCF-1-deficient, and β-catenin transgenic thymocytes to search for the genes that are down-regulated and up-regulated in TCF-1-deficient and β-catenin transgenic thymocytes, respectively. We focus on the genes that are significantly down-regulated and up-regulated in TCF-1-deficient and β-catenin transgenic thymocytes, respectively, to select for those genes that are potential target genes of β-catenin/TCF-1 pathway. And then those genes are subject to IPA pathway analysis searching for genes that are involved in thymocyte development and cell death.
2011-08-31 | E-GEOD-31371 | biostudies-arrayexpress
Project description:Both TCF-1 and its coactivator β-catenin are known to be required for supporting normal double positive (DP) thymocyte survival through upregulating Bcl-xL. However, the downstream factors mediating this effect remained unknown. We used microarray to compare the global expression difference among WT, TCF-1-deficient, and β-catenin transgenic thymocytes to search for the genes that are down-regulated and up-regulated in TCF-1-deficient and β-catenin transgenic thymocytes, respectively.
2011-09-01 | GSE31371 | GEO
Project description:The DNA binding factor Tcf-1 is one of the most prominently expressed genes in thymocytes yet its global DNA binding pattern remained unknown. Here we have assessed by ChIP-seq the Tcf-1 binding pattern in murine thymocytes in WT B6 mice and in mice expressing a stabilized form of the Tcf-1 binding partner beta-Catenin (CAT mice).
2013-06-12 | GSE46662 | GEO
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).
2012-10-25 | E-GEOD-33292 | biostudies-arrayexpress
Project description:Expression data from WT DN3, TCF-1-deficient DN3 thymocytes, and T cell lymphomas in TCF-1-deficient animals.
| PRJNA149283 | ENA
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.
2012-10-25 | GSE33292 | GEO
Project description:Unrestrained transcriptional activity of β-CATENIN and its binding partner TCF7L2 frequently underlies colorectal tumor initiation and is considered an obligatory oncogenic driver throughout intestinal carcinogenesis. Yet, the TCF7L2 gene carries inactivating mutations in about 10 % of colorectal tumors and is non-essential in colorectal cancer (CRC) cell lines. To determine whether CRC cells acquire TCF7L2-independence through cancer-specific compensation by other T-cell factor (TCF)/lymphoid enhancer‑binding factor (LEF) family members, or rather lose addiction to β-CATENIN/TCF7L2-driven gene expression altogether, we generated multiple CRC cell lines entirely negative for TCF/LEF or β-CATENIN expression. Viability of these cells demonstrates complete β‑CATENIN- and TCF/LEF-independence, albeit one β-CATENIN-deficient cell line eventually became senescent. Absence of TCF/LEF proteins and β-CATENIN consistently impaired CRC cell proliferation, reminiscent of mitogenic effects of WNT/β-CATENIN signaling in the healthy intestine. Despite this common phenotype, β-CATENIN-deficient cells exhibited highly cell-line-specific gene expression changes with little overlap between β-CATENIN- and TCF7L2-dependent transcriptomes. Apparently, β‑CATENIN and TCF7L2 control sizeable fractions of their target genes independently from each other. The observed divergence of β-CATENIN and TCF7L2 transcriptional programs, and the finding that neither β-CATENIN nor TCF/LEF activity is strictly required for CRC cell survival has important implications when evaluating these factors as potential drug targets.
2022-12-13 | GSE199835 | GEO
Project description:The Wnt signaling pathway is involved in many differentiation events during embryonic development and can lead to tumor formation after aberrant activation of its components. Β-catenin, a cytoplasmic component, plays a major role in the transduction of the canonical wnt/ β-catenin signaling. The aim of this study was to identify novel genes that are regulated by active β-catenin/TCF signaling in hepatocellular carcinoma. We selected and expanded isogenic clones from hepatocellular carcinoma-derived Huh7 cells with high and low β-catenin/TCF activities. We showed that, high TCF activity Huh7 cells lead to bigger and more aggressive tumors when xenografted into nude mice. We used SAGE (Serial Analysis of Gene Expression), genome-wide microarray and in silico promoter analysis in parallel, to compare gene expression between low (basal) and high (transfected) β-catenin/TCF activity clones, those had been xenografted into nude mice. We compared and contrasted SAGE and genome-wide microarray data, in parallel. Finally; after combined analysis, we identified BRI3 and HSF2 as novel targets of Wnt/β-catenin signaling in hepatocellular carcinoma. Experiment Overall Design: High TCF activity Huh7 cell line (Huh7-S33Y) was compared to control Huh7 cell line (Huh7-Vec) by using 10 ug of total RNA isolated from each sample (15 ug of labeled cRNA was hybridized to the arrays). Triplicates are coming from same total RNA extraction.
2009-10-10 | E-GEOD-11916 | biostudies-arrayexpress
Project description:Expression data from developing thymocytes of N15TCR transgenic Rag2 deficient mice
| PRJNA110173 | ENA
Project description:The Wnt signaling pathway is involved in many differentiation events during embryonic development and can lead to tumor formation after aberrant activation of its components. Β-catenin, a cytoplasmic component, plays a major role in the transduction of the canonical wnt/ β-catenin signaling. The aim of this study was to identify novel genes that are regulated by active β-catenin/TCF signaling in hepatocellular carcinoma. We selected and expanded isogenic clones from hepatocellular carcinoma-derived Huh7 cells with high and low β-catenin/TCF activities. We showed that, high TCF activity Huh7 cells lead to bigger and more aggressive tumors when xenografted into nude mice. We used SAGE (Serial Analysis of Gene Expression), genome-wide microarray and in silico promoter analysis in parallel, to compare gene expression between low (basal) and high (transfected) β-catenin/TCF activity clones, those had been xenografted into nude mice. We compared and contrasted SAGE and genome-wide microarray data, in parallel. Finally; after combined analysis, we identified BRI3 and HSF2 as novel targets of Wnt/β-catenin signaling in hepatocellular carcinoma.
2009-09-30 | GSE11916 | GEO