Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA157209 | ENA |
REPOSITORIES: ENA
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Project description:We present a computational method for building a regulatory network from global phosphoproteomic and transcription profiling data. To recover the critical missing links between signaling events and transcriptional responses, we relate changes in chromatin accessibility to changes in expression and then uses these links to connect proteomic and transcriptome data. We applied our approach to integrate epigenomic, phosphoproteomic and transcriptome changes induced by the variant III mutation of the epidermal growth factor receptor (EGFRvIII) in a cell line model of glioblastoma multiforme (GBM). Genome-wide DNase I hypersensitivity followed by sequencing (DNase-Seq) to measure chromatin accessibility in a cell line derived from the U87MG glioblastoma cell line to express high level of EGFRvIII (U87H; 2 million copies of EGFRvIII per cell) and a control cell line expressing kinase dead EGFRvIII (U87DK; 2 million kinase dead EGFRvIII per cell). A prediction from the computational method, the transcriptional co-regulator p300, was experimentally validated by chromatin immunoprecipitation followed by sequencing (ChIP-Seq).
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Project description:EGFRvIII is the most common deletion mutant of EGFR in human cancer and its levels are highly correlated with poor prognosis in GBM. The deletion of exons 2-7 removes most of the extracellular ligand binding domain, so it is unable to bind EGF or other EGFR-binding ligands. Nevertheless, the mutant receptor is constitutively phosphorylated, and is capable of activating downstream signaling pathways at a low level. To comprehensively identify the downstream signaling consequences of the EGFRvIII, we incorporated phosphoproteomic, transcription profiling and DNase-Seq data from U87MG glioblastoma cells expressing titrated levels of this mutant receptor.
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Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs. One-condition experment, gene expression of 3A6
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