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Effect of a gamma secretase inhibitor on the T29 cell line

ABSTRACT: The mouse Ikaros-deficient thymic lymphoma cell line T29 was treated with a gamma-secretase inhibitor or vehicle (DMSO) for 36h and subjected to transcriptome analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE46095 | GEO | 2013/04/17

SECONDARY ACCESSION(S): PRJNA197252

REPOSITORIES: GEO

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Effect of a gamma secretase inhibitor on the T29 cell line

Project description:The mouse Ikaros-deficient thymic lymphoma cell line T29 was treated with a gamma-secretase inhibitor or vehicle (DMSO) for 36h and subjected to transcriptome analysis. 4 samples

2013-04-17 | E-GEOD-46095 | biostudies-arrayexpress

Ikaros responsive genes in the T29 cell line

Project description:The mouse Ikaros-deficient thymic lymphoma cell line T29 was transduced with an empty retrovirus (MigR1) or a retrovirus expressing an fusion proein between Ikaros1 and the ligand binding domain of the estrogen receptor. Cells trreated with ethanol or 4-hydroxy-tamoxyfen (4OHT) for 24h were profiled. We used expression of an inducible ersion of the Ikaros protein in an Ikaros-deficient cell line to identify Ikaros-regulated genes

2013-04-17 | E-GEOD-46088 | biostudies-arrayexpress

Notch responsive genes in the T29 cell line

Project description:The mouse Ikaros-deficient thymic lymphoma cell line T29 was transduced with a retrovirus expressing an fusion protein between a dominant-negative form of Mastermind and the ligand binding domain of the estrogen receptor. Cells trreated with Ethanol or 4-hydroxy-tamoxyfen for 24h were profiled. We used expression of an inducible ersion of the dominant negative Mastermind protein in an Ikaros-deficient cell line to identify Notch-regulated genes

2013-04-17 | E-GEOD-46089 | biostudies-arrayexpress

Notch responsive genes in the T29 cell line

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2013-04-17 | GSE46088 | GEO

Identification of naturally short gamma-secretase substrates

Project description:The intramembrane protease gamma-secretase has broad physiological functions, but also contributes to Notch-dependent tumors and Alzheimer’s disease. To identify naturally short substrates and non-substrates of gamma-secretase, we used four human cell lines of different tissue origins, breast cancer MCF7 cells, cervix carcinoma HeLa cells, T cell leukemia Jurkat cells and lymphoma U937 macrophage-like cells. The cell lines were treated overnight with the established gamma-secretase inhibitor DAPT or DMSO as a control. The proteomes of membrane fractions were determined by nano-liquid chromatography-tandem mass spectrometry and label-free quantitative proteomics. TNFRSF12A, PTPRCAP and C16orf54 were identified as potential naturally short gamma-secretase substrates, whereas other proteins with a short ectodomain including ‘pituitary tumor-transforming gene 1-interacting protein’ (PTTG1IP) did not show an increased abundance upon DAPT treatment.

2024-05-24 | PXD045701 | Pride

Mapping of Ikaros and RBPJ binding sites in the mouse T cell leukemia cell line T29

Project description:The transcription factor Ikaros represses Notch signaling. Since Ikaros and Notch treanscriptional mediator RBPJ both recognize sequences that contain the same core TGGGAA motif, it was hypothesized that Ikaros represses Notch signaling by targeting Notch response elements and competing with RBPJ for their binding. Here we used the mouse T-cell leukemia cell line T29 to compare the genomic binding profiles of Ikaros and RBPJ by ChIP-seq. The T29 cell line is derived from a Ikaros-deficient T-cell leukemia (Dumortier et al, MCB 26, 209-220, 2006) and exhibits strong Notch activation. We performed two chip-seq experiments with an anti-RBPJ antibody to map RBPJ binding sites. To map Ikaros binding sites, we engineered a T29-derived cell line that expresses a fusion protein between Ikaros and the ligand binding domain of the estrogen receptor (Ik1-ER) which is activated by addition of 4-hydroxy-tamoxifen (4OHT). We used an anti-Ikaros antibody to map the sites bound by Ik1-ER after treatment of the cells with 4OHT. Sequencing were performed with the Illumina GAII sequencer as as single end 36 base pair reads.

2014-04-02 | E-GEOD-46119 | biostudies-arrayexpress

Mapping of Ikaros and RBPJ binding sites in the mouse T cell leukemia cell line T29

2014-04-02 | GSE46119 | GEO

Alteration in global transcriptome after Notch inhibition with gamma-secretase inhibitor MRK003 in Glioblastoma Cells

Project description:We used DNA microarrays to compare RNA transcript expression from various glioma neurospheres after treatment with gamma-secretase inhibitor MRK003. Four glioma cell lines grown as neurospheres (GBM1, GBM2, GBM10 and GBM14) were treated two concentrations of with gamma-secretase inhibitor MRK003 (High and low dose, 0.4µM and 2.0µM respectively) and compared to vehicle (DMSO) control. Whole human genome gene expression was performed at the Johns Hopkins Oncology Microarray Core using 44k microarray technology (Agilent Technologies, CA, USA) according to manufacturer’s description including labeling, hybridization and detection. Gene annotation and expression analyses were performed using software packages available from the R/Bioconductor platform for statistical computing. In this series we provide raw expression data along with MIAME (Minimal Information about a Microarray Experiment).

2015-08-07 | E-GEOD-71769 | biostudies-arrayexpress

Genes regulated by the gamma secretase inhibitor in WT and Ikaros deficient DN3 cells

Project description:Lineage-negative thymocytes were cultured on OP9-DL1 stromal cells for 16h in the presence of DMSO or the gamma secretase inhibitor MRK-003. DN3 cells cells were then sorted and their transcriptome analyzed.

2013-04-17 | GSE46091 | GEO

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