Gtf2i and Gtf2ird1 E13.5 whole brain ChIP-seq and RNA-seq
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ABSTRACT:
PROVIDER: PRJNA575176 | ENA |
REPOSITORIES: ENA
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Project description:HetxHet breeding pairs for the Gtf2i/Gtf2ird1 double mutants and Gtf2ird1 were set up for timed breedings. E13.5 embyros of WT, HET, and HOM mutants (n=3 for each genotype and each cross), were used for RNA-seq. Similar breedings were done for ChIP-seq. The ChIP-seq WT controls were E13.5 embyros from WT FVB/ANTJ x FVB/ANTJ and compared to HOM Gtf2i/Gtf2ird1 double mutatns and HOM Gtf2ird1 single mutants. There were n=3 WT and n=3 hom Gtf2ird1 single mutants for Gtf2ird1 ChIP-seq. There were n=4 WT and n=4 hom Gtf2i/Gtf2ird1 double mutants for Gtf2i ChIP-seq. Each genotype had the sample matched input control along with ChIP sample.
2020-11-11 | GSE138234 | GEO
Project description:HITS-CLIP is performed for the RNA-binding protein, IMP2/IGF2BP2, from E13.5 mouse brain.
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Project description:IMP2/IGF2BP2 HITS-CLIP from E13.5 mouse brain
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Project description:Transcriptional profiling of mouse cortex tissue comparing control animals with Gtf2i-mutated mouse (Gtf2i+/Δex2 ). Goal was to determine the specific deregulated genes in the cortex of mutated animals.
2014-10-20 | GSE41251 | GEO
Project description:Data present the expression analysis of different mouse ES cell line with altered expression of GTF2I. We used microarrays to detail the global programme of gene expression underlying altered expression of GTF2I and identified distinct classes of deregulated genes
2013-07-12 | E-GEOD-48790 | biostudies-arrayexpress
Project description:The pathogenesis of thymic epithelial tumors (TETs) is poorly understood. Recently we reported the frequent occurrence of a missense mutation in the GTF2I gene in TETs and hypothesized that GTF2I mutation might contribute to thymic tumorigenesis. Expression of mutant TFII-I altered the transcriptome of normal thymic epithelial cells and upregulated several oncogenic genes. Gtf2i L424H knockin cells exhibited cell transformation, aneuploidy, and increase tumor growth and survival under glucose deprivation or DNA damage. Gtf2i mutation also increased the expression of several glycolytic enzymes, cyclooxygenase-2, and caused modifications of lipid metabolism. Elevated cyclooxygenase-2 expression by Gtf2i mutation was required for survival under metabolic stress and cellular transformation of thymic epithelial cells. Our findings identify GTF2I mutation as a new oncogenic driver that is responsible for transformation of thymic epithelial cells.
2022-03-02 | GSE127909 | GEO
Project description:Transcriptional profiling of mouse cortex tissue comparing control animals with Gtf2i-mutated mouse (Gtf2i+/Δex2 ). Goal was to determine the specific deregulated genes in the cortex of mutated animals. Pools of total RNA derived from five-three mice of each genotype were subjected to microarray analysis. We compared pools instead of single individuals in order to minimize individual and technically-related variation. The original raw data file (i.e. Agilent feature extraction files) are not available. The modified raw data files are provided along with the file contents description (raw_data_readme.txt available on Series records).
2014-10-20 | E-GEOD-41251 | biostudies-arrayexpress
Project description:The molecular mechanisms underlying the pathogenesis of TETs are poorly understood. Recently we reported a common missense mutation on GTF2I gene in thymic tumors and hypothesized that GTF2I mutation might contribute to thymic tumorigenesis. Expression of mutant TFII-I altered the transcriptome of thymic epithelial cells and up-regulated several oncogenic genes. Using CRISPR/Cas9n, Gtf2i T1211A knock-in cells exhibited distinct features of cancerous cells including cell transformation, aneuploidy, tumor growth in xenograft, and survival after DNA damage or glucose deprivation. We also observed that Gtf2i mutation increased the expression of several glycolytic enzymes, cyclooxygenase-2, and altered lipid metabolism. Elevated COX-2 expression by Gtf2i mutation was required for survival under metabolic stress and cellular transformation of thymic epithelial cells. Our findings identify GTF2I mutation as a new oncogenic driver mutation that is responsible for transformation of thymic epithelial cells.
2022-03-02 | GSE127908 | GEO
Project description:The molecular mechanisms underlying the pathogenesis of TETs are poorly understood. Recently we reported a common missense mutation on GTF2I gene in thymic tumors and hypothesized that GTF2I mutation might contribute to thymic tumorigenesis. Expression of mutant TFII-I altered the transcriptome of thymic epithelial cells and up-regulated several oncogenic genes. Using CRISPR/Cas9n, Gtf2i T1211A knock-in cells exhibited distinct features of cancerous cells including cell transformation, aneuploidy, tumor growth in xenograft, and survival after DNA damage or glucose deprivation. We also observed that Gtf2i mutation increased the expression of several glycolytic enzymes, cyclooxygenase-2, and altered lipid metabolism. Elevated COX-2 expression by Gtf2i mutation was required for survival under metabolic stress and cellular transformation of thymic epithelial cells. Our findings identify GTF2I mutation as a new oncogenic driver mutation that is responsible for transformation of thymic epithelial cells.
2022-03-02 | GSE127907 | GEO