Ontology highlight
ABSTRACT:
PROVIDER: PRJNA253776 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Phosphoproteome analysis from BCR-ABL, MYC and CD22DE12 transgenic mouse models
| PRJNA253778 | ENA
Project description:We have compared the gene expression profiles of leukemic tissues in two different mouse models of AML, CALM-AF10 and NHD13, to clincally healthy transgenic and wildtype hematopoetic tissue to identify genes and pathways that can collaborate with these oncogenic fusion proteins to promote leukemic transformation.
2012-09-01 | GSE40531 | GEO
Project description:We have compared the gene expression profiles of leukemic tissues in two different mouse models of AML, CALM-AF10 and NHD13, to clincally healthy transgenic and wildtype hematopoetic tissue to identify genes and pathways that can collaborate with these oncogenic fusion proteins to promote leukemic transformation. CA10 and NHD13 transgenic mice were sacrificed when clinical signs of leukemia manifested (mice were hunched, skinny, or had an abnormal complete blood count). For comparsion, we harvested age matched bone marrow, thymi, and spleen from wildtype and clinically healthy trangenic tissues. Transgenic animals were considered clinically healthy if no evident signs of leukemia were present.
2012-09-01 | E-GEOD-40531 | biostudies-arrayexpress
Project description:The TEL-JAK2 fusion oncogene and the ICN1 activated allele of NOTCH1 are the result of specific chromosomal translocations in T cell acute lymphoblastic leukemia (T-ALL). Mouse models of these diseases (TEL-JAK2 transgenic mice; Carron C. et al. Blood (2000); a bone marrow transplantation model for ICN1-induced T-ALL) were used to compare the transcriptional program specific to each oncoprotein in mouse models of these leukemias. Tumor load was >50% leukemic cells in all selected organs. Leukemic cells were collected from the thymus of terminally-ill TEL-JAK2 leukemic mice and bone marrow of terminally-ill ICN1 leukemic mice. RNA was extracted from each sample and processed for hybridization to Affymetrix arrays.
2013-09-28 | E-GEOD-51243 | biostudies-arrayexpress
Project description:We have developed a new conditional transgenic mouse showing that MLL-ENL, at an endogenous-like expression level, induces leukemic transformation selectively in LT-HSCs. To investigate the molecular mechanism of leukemic transformation in LT-HSCs conditionally expressing MLL-ENL, we preliminarily performed comprehensive gene expression profiling of CreER-transduced LT-HSCs and ST-HSCs using cDNA microarray analysis.
2013-07-17 | GSE48539 | GEO
Project description:<p>RNA sequencing was performed on human DRGs and relative gene abundances were calculated.</p> <p>Various analyses were performed:</p> <p> <ol> <li>Human DRG gene expression profiles were contrasted with a panel of gene expression profiles of relevant tissues in human and mouse ( integrating, among other sources, datasets from ENCODE and GTex ) in order to identify.</li> <ol type="a"> <li>DRG-enriched gene expression, co-expression modules of DRG-expressed genes, and key transcriptional regulators in humans.</li> <li>Contrasting the human and mouse DRG transcriptomes to identify DRG-enriched gene expression patterns that were conserved between human and mouse, identifying putative cell types of expression of these genes, and potential known drugs that might target the corresponding gene products.</li> <li>Characterization of non-coding RNA profile of human and mouse DRGs.</li> <li>Characterization of DRG-enriched alternative splicing and alternative transcription start site usage based transcript variants in humans and mouse, and the overlap between these two species.</li> <li>Contrasting of human DRG and GTex human tibial nerve samples to identify putative axonally transported mRNAs in sensory neurons.</li> </ol> <li>Human DRG transcriptomes from donors suffering from neuropathic and/or chronic pain were contrasted with controls to identify.</li> <ol type="a"> <li>Differentially expressed genes, pathways and regulators path play a potential role in neuronal plasticity, electrophysiological activity, immune signaling and response.</li> <li>Predictive models (Random Forests) were built to jointly predict the sex and pain state of samples based on information contained solely in autosomal gene expression profile.</li> <li>Gene co-expression modules were identified and gene set enrichment analysis performed.to identify sample - pathway associations, and to broadly characterize plasticity in human DRG cell types.</li> </ol> </ol> </p>
| phs001158 | dbGaP
Project description:The TEL-JAK2 fusion oncogene and the ICN1 activated allele of NOTCH1 are the result of specific chromosomal translocations in T cell acute lymphoblastic leukemia (T-ALL). Mouse models of these diseases (TEL-JAK2 transgenic mice; Carron C. et al. Blood (2000); a bone marrow transplantation model for ICN1-induced T-ALL) were used to compare the transcriptional program specific to each oncoprotein in mouse models of these leukemias. Tumor load was >50% leukemic cells in all selected organs.
2013-09-28 | GSE51243 | GEO
Project description:Primary outcome(s): Cancer related genome analysis, gene expression and molecular characterization analysis
| 2647002 | ecrin-mdr-crc
Project description:Type I interferons (IFN-Is) are immunoregulatory cytokines that are essential for normal host antiviral responses. The current understanding is that IFN-Is mediate their effects through the expression of several hundred interferon-regulated genes. Here we identified a novel IFN-I response mechanism that relies on widespread changes in protein phosphorylation. IFN-I-induced phosphorylation in primary murine microglia and astrocytes – key IFN-I-responding cells of the central nervous system – was rapid and thus largely independent of gene expression. Based on in silico analysis, this mechanism relies predominantly on a small number of kinase families. Further, functional analysis suggested that this rapid response induces an immediate reactive state in cells and prepares them for the subsequent transcriptomic response. Similar extensive phosphoproteome changes were also present in a mouse model for IFN-I-induced neuroinflammatory diseases. Strikingly, the altered phosphoproteome in these transgenic mice predicted the clinical and pathological outcome of neuroinflammatory disease. These findings demonstrate for the first time a novel mechanism by which IFN-Is mediate cellular responses.
2021-11-02 | PXD014443 | Pride
Project description:Here, we investigated the neurodevelopmental impact of Ube3a gene overdosage using bacterial artificial chromosome-based transgenic mouse models (Ube3aOE) that recapitulate the increases in Ube3a copy number most often observed in Dup15q.Here, we investigated the neurodevelopmental impact of Ube3a gene overdosage using bacterial artificial chromosome-based transgenic mouse models (Ube3aOE) that recapitulate the increases in Ube3a copy number most often observed in Dup15q. Hereto we performed gene expression profiling analysis using data obtained from RNA-seq of cortical and hippocampal tissue from wildtype and Ube3aOE mice
2022-08-04 | GSE205128 | GEO