Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA147833 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human T-cell Acute lymphoblastic Leukemia cell line CEM was transfected with either shRNA against ZMIZ1 or scrambled shRNA. Four (non-paired) biological replicates of each condition had mRNA assays performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets. A supplementary Excel workbook holding the same processed data as the series matrix file is provided, with some probe set annotation, and a simple statistical comparison. The raw (.CEL) files are also provided. Keywords: Expression profiling by array Human T-cell Acute lymphoblastic Leukemia cell line CEM was transfected with either shRNA against ZMIZ1 or scrambled shRNA. Four (non-paired) biological replicates of each condition had mRNA assays performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets.
2012-12-13 | E-GEOD-32523 | biostudies-arrayexpress
Project description:Human T-cell Acute lymphoblastic Leukemia cell line CEM was transfected with either shRNA against ZMIZ1 or scrambled shRNA. Four (non-paired) biological replicates of each condition had mRNA assays performed using Affymetrix HG_U133_plus_2 arrays, with 54675 probe-sets. A supplementary Excel workbook holding the same processed data as the series matrix file is provided, with some probe set annotation, and a simple statistical comparison. The raw (.CEL) files are also provided. Keywords: Expression profiling by array
2012-12-13 | GSE32523 | GEO
Project description:The most recurrently mutated oncogene in T-cell acute lymphoblastic leukemia (T-ALL) is NOTCH1. The core Notch complex consists of an ICN protein, a Maml cofactor, and the DNA binding factor Rbpj. The known direct cofactors of Notch appear to act nonselectively, homogeneously driving Notch gene expression functions. It is unclear whether there are direct cofactors of Notch that act selectively and heterogeneously regulate ICN. We discovered that Zmiz1, a Protein Inhibitor of Activated STAT (PIAS)-like coactivator, directly bound ICN1. ChIP-Seq showed that Zmiz1 selectively co-bound only a subset of Notch-regulated enhancers. This led to hypothesize that Zmiz1 regulates only a subset of Notch1 target genes. To investigate this, we performed RNA-Seq on four 8946 cell linesin which L1601P (activated Notch1) or Zmiz1 were expressed alone or in combination. Zmiz1 induced ~10% of Notch target genes. The Notch target gene that was most strongly induced by Zmiz1 was Myc. Our data suggest that Zmiz1 selectively amplifies a subset of Notch target genes with strong amplification of Myc. RNA-Seq in a murine T-ALL cell line
2015-10-28 | E-GEOD-66145 | biostudies-arrayexpress
Project description:The most recurrently mutated oncogene in T-cell acute lymphoblastic leukemia (T-ALL) is NOTCH1. The core Notch complex consists of an ICN protein, a Maml cofactor, and the DNA binding factor Rbpj. The known direct cofactors of Notch appear to act nonselectively, homogeneously driving Notch gene expression functions. It is unclear whether there are direct cofactors of Notch that act selectively and heterogeneously regulate ICN. We discovered that Zmiz1, a Protein Inhibitor of Activated STAT (PIAS)-like coactivator, directly bound ICN1. In order to determine whether this interaction occured at chromatin, we performed ChIP-Seq. We identified significant overlap between ICN1, Rbpj, and Zmiz1 peaks. 75% of overlapping ICN1/Rbpj peaks overlapped with Zmiz1 (HA) peaks (273 peaks). The size of Zmiz1 (HA) peaks had moderate correlation with the size of Rbpj and ICN1 peaks. Like Rbpj and ICN1 peaks, Zmiz1 (HA) peaks were associated with activating H3K27ac, H3K4me1, and H3K4me3 chromatin marks and were devoid of repressive H3K27me3 marks. These data suggest that Zmiz1 is a selective Notch regulator. It co-binds only a subset of ICN1 and Rbpj-regulated sites. Zmiz1, ICN1, Rbpj, histone mehylation ChIP-Seq in murine T-ALL cell line
2015-10-28 | E-GEOD-66146 | biostudies-arrayexpress
Project description:STAT3 (Signal transducer and activator of transcription 3) expression is associated with with t(12;21) acute lymphoblastic leukaemia (ALL) and it is crucial for the survival of the t(12;21) ALL . Our study investigated the STAT3 regulated pathways and discovered a novel STAT3-TP53 axis in B-ALL. In order to determine the STAT3 regulated pathways in t(12;21) ALL cells, we performed RNAseq analysis on the Pre-B Acute Lymphoblastic Leukemia (ALL) cell line REH following shRNA-mediated STAT3 knockdown
2024-01-31 | GSE179332 | GEO
Project description:To study the effect of PPM1A-AS on T-cell acute lymphoblastic leukemia (T-ALL) cells, we conducted shRNA-mediated knockdown of PPM1A-AS in Jurkat and performed RNA-seq.
2021-10-19 | GSE182998 | GEO
Project description:Four acute lymphoblastic leukemia cell lines SUP-B15, JURKAT, MOLT-3, and CCRF-CEM cells were treated with glucocorticoids such as dexamethasone and prednisolone for six hours before RNA extraction.
2020-12-18 | E-MTAB-9250 | biostudies-arrayexpress
Project description:Resistance to asparaginase, an antileukemic enzyme that depletes asparagine, is a common clinical problem. Using a genome-wide CRISPR/Cas9 screen, we found a synthetic lethal interaction between Wnt pathway activation and asparaginase in acute leukemias resistant to this enzyme. Wnt pathway activation induced asparaginase sensitivity in distinct treatment-resistant subtypes of acute leukemia, but not in normal hematopoietic progenitors. Sensitization to asparaginase was mediated by Wnt-dependent stabilization of proteins (Wnt/STOP), which inhibits GSK3-dependent protein ubiquitination and proteasomal degradation, a catabolic source of asparagine. Inhibiting the alpha isoform of GSK3 phenocopied this effect, and pharmacologic GSK3 inhibition profoundly sensitized drug-resistant leukemias to asparaginase. Our findings provide a molecular rationale for activation of Wnt/STOP signaling to improve the therapeutic index of asparaginase. To gain further insights into mechanisms of cytotoxicity of this combination, we applied unbiased mass spectrometry proteomics to CCRF-CEM cells, a human T-cell acute lymphoblastic leukemia cell line, treated with vehicle, asparaginase alone, the GSK3 inhibitor BRD0705 (which phenocopies Wnt/STOP pathway activation), or the combination of asparaginase and BRD0705.
2019-03-29 | PXD013061 | Pride
Project description:Two human acute lymphoblastic leukemia cell lines (Molt-4 and CCRF-CEM) were treated with direct (A-769662) and indirect (AICAR) AMPK activators. Molt-4 and CCRF-CEM cells were obtained from ATCC (CRL-1582 and CCL-119). Control samples were used for the analysis of metabolic differences between cell lines. Therefore the data was analyzed in combination with, metabolomic data, and the genome-scale reconstruction of human metabolism. For experiments cells were grown in serum-free medium containing DMSO (0.67%) at a cell concentration of 5 x 105 cells/mL.
2014-12-31 | GSE53123 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE29179: Identification of differentially expressed genes upon shRNA knockdown of TAL1 and its regulatory partners in T-ALL cells (Jurkat) GSE29180: ChIP-Seq of TAL1 and its regulatory partners in T-ALL cells (Jurkat) GSE33850: Core transcriptional regulatory circuit controlled by the tal1 complex in human t-cell acute lymphoblastic leukemia (Subseries) Refer to individual Series
2012-08-16 | E-GEOD-29181 | biostudies-arrayexpress