Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA290332 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from isogenic Pten WT mouse T-ALLs infected with MSCV Myr-AKT-IRES-mCherry or empty vector, treated with DBZ or DMSO
| PRJNA290331 | ENA
Project description:To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo. This analysis revealed that, while direct NOTCH1 target genes (such as Hes1, Dtx1, PtcrA, HeyL and Notch3) are effectively downregulated in both Pten-positive and Pten-deleted tumors, genetic ablation of Pten elicits a global reversal of much of the transcriptional effects of NOTCH inhibition. We performed microarray gene expression analysis of GSI treatment in isogenic Pten KO or WT NOTCH1 induced leukemias
2015-08-31 | E-GEOD-71087 | biostudies-arrayexpress
Project description:To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo. This analysis revealed that, while direct NOTCH1 target genes (such as Hes1, Dtx1, PtcrA, HeyL and Notch3) are effectively downregulated in both Pten-positive and Pten-deleted tumors, genetic ablation of Pten elicits a global reversal of much of the transcriptional effects of NOTCH inhibition.
2015-08-31 | GSE71087 | GEO
Project description:The goal of this study is to compare gene expression profiles of PTEN WT and KO GBM cells when they are growing in vivo. Isogenic PTEN WT or KO LN229 GBM cells were subcutaneously implanted into Balb/c nude mice (two in each group) to form tumor. At the 30th day tumors were harvested and total RNA was isolated. RNA-seq analysis was performed to examine the differential express pattern of the two type of xenografts.
2019-09-04 | GSE136738 | GEO
Project description:Basal cells were isolated from an influenza-infected non-tamoxifen treated Krt5CreERT2; RFP; ∆Np63flox/flox mouse and cultured, allowing for inducible ∆Np63 deletion in vitro. These basal cells were plated as monolayers and treated with 1uM 4OHT for +4OHT (∆Np63 KO) or equivalent volume DMSO for -4OHT (solvent only, ∆Np63 WT) for 48 hours. Technical triplicates of ∆Np63 WT and ∆Np63 KO treated in parallel were harvested for each IP for p63 and each histone modification for ChIP-seq.
2022-11-11 | GSE216159 | GEO
Project description:Basal cells were isolated from an influenza-infected non-tamoxifen treated Krt5CreERT2; RFP; ∆Np63flox/flox mouse and cultured, allowing for inducible ∆Np63 deletion in vitro. These basal cells were plated as monolayers, airway organoids, and alveolar organoids and treated with 1uM 4OHT for +4OHT (∆Np63 KO) or equivalent volume DMSO for -4OHT (solvent only, ∆Np63 WT). Technical triplicates of ∆Np63 WT and ∆Np63 KO were harvested for each growth condition for RNA sequencing.
2022-11-11 | GSE216160 | GEO
Project description:NOTCH1 is a transcription factor involved in T-cell development and mutations that occur in NOTCH1 gene affects more than 60% of patients affected by T-cell acute lymphoblastic leukemia (T-ALL). In order to identify microRNAs regulated following NOTCH1 inhibition in T-ALL, murine NOTCH1-induced T-cell leukemia were treated with a NOTCH1 inhibitor (DBZ, Dibenzazepine). Tumors were established in irradiated C57BL/6 mice injected with lineage negative progenitors cells transduced with a mutated NOTCH1 allele (HD-ΔPEST NOTCH1). Mice were treated three times, 8 hours apart, with vehicle only (DMSO) or DBZ (5mg/Kg). Total RNA was extracted from tumor samples (spleens of sick mice) and hybridized on Agilent mouse miRNA 8x60K arrays (release 19.0). Each sample was derived from a different mouse (n=3 mice/group). Raw microarray data, preprocessed data matrix and results of differential expression analysis are available together with the applied protocols.
2020-07-30 | E-MTAB-9278 | biostudies-arrayexpress
Project description:NOTCH1 is a transcription factor involved in T-cell development and mutations that occur in NOTCH1 gene affects more than 60% of patients affected by T-cell acute lymphoblastic leukemia (T-ALL). In order to identify genes and pathways regulated following NOTCH1 inhibition in T-ALL, murine NOTCH1-induced T-cell leukemia were treated with a NOTCH1 inhibitor (DBZ, Dibenzazepine). Tumors were established in irradiated C57BL/6 mice injected with lineage negative progenitors cells transduced with a mutated NOTCH1 allele (HD-ΔPEST NOTCH1). Mice were treated three times, 8 hours apart, with vehicle only (DMSO) or DBZ (5mg/Kg). Total RNA was extracted from tumor samples (spleens of sick mice) and hybridized on Agilent SurePrint G3 Mouse GE 8x60K arrays. Each sample was derived from a different mouse (n=3 mice/group). Raw microarray data and results of differential expression analysis are available together with the applied protocols.
2020-07-30 | E-MTAB-9279 | biostudies-arrayexpress
Project description:To elucidate the role of SIRT1 in adult neural stem cells, we have carried out a genome-wide microarray analysis on cultured adult neurospheres from wildtype (WT) and sirt1 knockout (KO) mice and WT neurospheres treated with DMSO and SIRT1 activator,resveratrol for 24 hours. Then we screened for genes that exhibited opposite changing patterns beween KO-versus-WT and resveratrol-versus-DMSO-treated groups. Our result revealed a significant enrichment of genes involved in metabolic process. And numerous genes involved in cell proliferation and differentiation were represented in these SIRT1-responsive genes. More interestingly, Notch signaling-related genes,such as Dll4, Mib1,Hes5, Heyl, Hey2 and so on, also showed a significant enrichment. Real-time PCR validated the expression of Notch signaling-related genes. These data revealed the regulation of SIRT1 on the self-renewal and differentiation of adult neural stem cells.
2015-03-30 | GSE39551 | GEO