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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Calcineurin-dependent transcriptome in ICN1 (activated NOTCH1)-induced T cell acute lymphoblastic leukemia (T-ALL)

ABSTRACT: Activated NOTCH1 induces T-ALL in mice when transduced in bone marrow (BM) cells. T-ALL cells activate the calcineurin/NFAT pathway in vivo (Medyouf H. et al. Nat Med 2007 [PMID 17515895]). Through appropriate crosses, mouse ICN1-induced T-ALL were generated that include a ROSCreERT2 transgene and 2 copies of a CnB1 floxed alleles. Cohorts of secondary recipient mice were injected with these T-ALL cells, and when becoming leukemic, divided into 2 subgroups. Group 1 was treated with Tamoxifen (TAM), resulting in CnB1 gene deletion and inactivation of calcineurin. Group 2 was treated with carrier solvent (corn OIL), thus maintaining CnB1 and calcineurin activity. RNAs were extracted from flow cytometry-sorted leukemic cells. Details in Gachet S. et al. Leukemia 2013 (PMID 23689515).

ORGANISM(S): Mus musculus

SUBMITTER: Jacques GHYSDAEL

PROVIDER: E-GEOD-60258 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Calcineurin-dependent transcriptome in ICN1 (activated NOTCH1)-induced T cell acute lymphoblastic leukemia (T-ALL)

Project description:Activated NOTCH1 induces T-ALL in mice when transduced in bone marrow (BM) cells. T-ALL cells activate the calcineurin/NFAT pathway in vivo (Medyouf H. et al. Nat Med 2007 [PMID 17515895]). Through appropriate crosses, mouse ICN1-induced T-ALL were generated that include a ROSCreERT2 transgene and 2 copies of a CnB1 floxed alleles.

2014-08-09 | GSE60258 | GEO

Comparison of the transcriptome of TEL-JAK2- versus activated NOTCH1 (ICN1)-induced T cell acute lymphoblastic leukemias (mouse)

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

Comparison of the transcriptome of TEL-JAK2- versus activated NOTCH1 (ICN1)-induced T cell acute lymphoblastic leukemias (mouse)

2013-09-28 | GSE51243 | GEO

HDXMS of PI4KIIIa and Calcineurin

Project description:Using HDX-MS to reveal the binding sites of Calcineurin and PI4KIIIa

2021-09-22 | PXD025900 | Pride

Genome-wide analysis of intracellular notch1(ICN1) targets in gamma delta T cells (gd T cells).

Project description:We performed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq) for ICN1 in thymic gd T cells from neonates of C57BL/6 mice. Sequence reads for ICN1 and Input were aligned with the mouse reference genome (mm10) by bowtie program (v1.0.0), and peak detection and identification of ICN1 binding sites were obtained with MACS program (v1.4.2). ChIP-seq data revealed that 12%, 6% and 47% of ICN1 binding sites were within -10kb upstream of transcription start site, +10kb downstream of 3'end and the bodies of genes, respectively. The other of ICN1 binding sites was intergenic. We also found that ICN1 directly bound -5.4kb upstream of transcript start site of IL-7 receptor alpha (IL-7Ra) locus, which were estimated as a new promoter region of IL-7Ra. Some of ICN1 binding sites (e.g. TCF1 promoter) were consistent with previous reports, but others (e.g. Nr4a1 promoter) were novel. These suggests that ICN1 was associated with a lot of transcriptional regulation in gd T cells.

2014-11-14 | GSE56756 | GEO

Genome-wide analysis of intracellular notch1(ICN1) targets in gamma delta T cells (gd T cells).

2014-11-14 | E-GEOD-56756 | biostudies-arrayexpress

Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells following Ikaros restoration

Project description:To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL211) cells isolated from two untreated and two 3-day Dox-treated mice.

2015-02-02 | E-GEOD-64899 | biostudies-arrayexpress

Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL65) cells following Ikaros restoration

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2015-02-02 | E-GEOD-64893 | biostudies-arrayexpress

Expression profiling of mouse T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL101) cells following Ikaros restoration [RNA-Seq]

Project description:To examine Ikaros tumor suppressor mechanisms, we have utilized inducible RNAi to dynamically restore endogenous Ikaros expression in T-ALL driven by its knockdown. This causes rapid transcriptional repression of Notch1 and associated targets including Myc, even in leukemias harboring spontaneous activating Notch1 mutations (producing aberrant ICN1) similar to those found in 60% of human T-ALL. Ikaros restoration results in sustained regression of Notch1-wild type leukemias while endogenous or engineered ICN1 expression promotes rapid disease relapse, indicating that ICN1 functionally antagonizes Ikaros in T-ALL. RNA-seq was performed on T-ALL (Vav-tTA;TRE-GFP-shIkaros primary leukemia ALL101) cells isolated from three untreated and three 3-day Dox-treated mice. There were two sequencing runs of each RNA sample.

2015-02-02 | E-GEOD-54447 | biostudies-arrayexpress

The Polycomb Repressive Complex 2 Is Required For MLL-AF9 Leukemia

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2012-02-22 | E-GEOD-34963 | biostudies-arrayexpress

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