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GSE65384
Mus musculus
26 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MLL-AF9 Expression in Hematopoietic Stem Cells Drives a Highly Invasive AML Expressing EMT-Related Genes Linked to Poor Outcome.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 23 Downloadable Samples
Illumina HiSeq 2000
Description
To address the impact of cellular origin on AML, we generated an inducible transgenic mouse model for MLL-AF9 driven leukemia. MLL-AF9 expression in long-term hematopoietic stem cells (LT-HSCs) in vitro resulted in unprecedented clonogenic growth and expression of genes involved in migration and invasion. In vivo, some LT-HSC-derived AMLs were particularly aggressive with extensive tissue infiltration, chemo-resistance and expression of genes related to epithelial-mesenchymal transition (EMT) in solid cancers. Knockdown of the EMT regulators Zeb1 and Tcf4 significantly reduced leukemic blast invasion. By classifying mouse and human leukemia according to Evi1/EVI1and Erg/ERG expression, reflecting aggressiveness and cell-of-origin and performing comparative transcriptomics we identified numerous EMT-related genes that were significantly associated with poor overall survival of AML patients. Overall design: RNA from FACS sorted bone marrow subpopulations was isolated, RNA-sequencing libraries were prepared and sequenced on an Illumina HiSeq 2000. Reads mapping to RefSeq transcripts were counted.
Publication Title
MLL-AF9 Expression in Hematopoietic Stem Cells Drives a Highly Invasive AML Expressing EMT-Related Genes Linked to Poor Outcome.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
To address the impact of cellular origin on AML, we generated an inducible transgenic mouse model for MLL-AF9 driven leukemia. MLL-AF9 expression in long-term hematopoietic stem cells (LT-HSCs) in vitro resulted in unprecedented clonogenic growth and expression of genes involved in migration and invasion. In vivo, some LT-HSC-derived AMLs were particularly aggressive with extensive tissue infiltration, chemo-resistance and expression of genes related to epithelial-mesenchymal transition (EMT) in solid cancers. Knockdown of the EMT regulators Zeb1 and Tcf4 significantly reduced leukemic blast invasion. By classifying mouse and human leukemia according to Evi1/EVI1and Erg/ERG expression, reflecting aggressiveness and cell-of-origin and performing comparative transcriptomics we identified numerous EMT-related genes that were significantly associated with poor overall survival of AML patients.
Publication Title
MLL-AF9 Expression in Hematopoietic Stem Cells Drives a Highly Invasive AML Expressing EMT-Related Genes Linked to Poor Outcome.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 28 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Tumor tissue heterogeneity is a well known feature of several solid tumors. Neuroblastic Tumors (NTs) is a group of paediatric cancers with a great tissue heterogeneity. Most of NTs are composed of undifferentiated, poorly differentiated or differentiating neuroblastic (Nb) cells with very few or absent Schwannian stromal (SS) cells: these tumors are grouped as Neuroblastoma (Schwannian stroma-poor). The remaining NTs are composed of abundant SS cells and classified as Ganglioneuroblastoma (Schwannian stroma-rich) intermixed or nodular and Ganglioneuroma. The importance to understand Nb and SS gene signatures in NTs, is to clarify the complex network mechanism of tumor growth and progression. In order to identify the Nb and SS cells gene signatures, we analyzed the gene expression profiling of 19 cases of neuroblastic tumors: 10 stroma poor (NTs-SP) and 9 stroma rich (NTs-SR), by high density oligonucleotide microarrays. Moreover, the analysis was performed in parallel on both whole and laser microdissected tumor samples: from 4 of 19 cases, was isolated different areas all composed of pure cellular populations.
Publication Title
Identification of low intratumoral gene expression heterogeneity in neuroblastic tumors by genome-wide expression analysis and game theory.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
Neurons exploit mRNA localization and local translation to spatio-temporally regulate gene expression during development. Local translation and retrograde transport of transcription factors regulate nuclear gene expression in response to signaling events at distal neuronal ends. Whether epigenetic factors could also be involved in such regulation is not known. We report that the mRNA encoding the high mobility group N5 (HMGN5) chromatin binding protein localizes to growth cones of both neuronal-like cells and of hippocampal neurons. We show that Hmgn5 3UTR drives growth cone localization and translation of a reporter gene, and that HMGN5 can be retrogradely transported into the nucleus along neurites. Loss of HMGN5 function induces transcriptional changes and impairs neurite outgrowth while HMGN5 overexpression induces neurite outgrowth and global chromatin decompaction. Interestingly, control of both neurite outgrowth and chromatin structure is dependent on proper growth cone localization of Hmgn5 mRNA. Our results provide the first evidence that mRNA localization and local translation might serve as a mechanism to couple the dynamic neuronal outgrowth process with chromatin regulation in the nucleus.
Publication Title
Growth Cone Localization of the mRNA Encoding the Chromatin Regulator HMGN5 Modulates Neurite Outgrowth.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 13 Downloadable Samples
- Affymetrix Multispecies miRNA-3 Array (mirna3), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Surgery-Induced Weight Loss Is Associated With the Downregulation of Genes Targeted by MicroRNAs in Adipose Tissue.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Homo sapiens
- 13 Downloadable Samples
Affymetrix Human Gene 2.0 ST Array (hugene20st), Affymetrix Multispecies miRNA-3 Array (mirna3)
Description
Molecular mechanisms associated with pathophysiological variations in adipose tissue (AT) are not fully recognized. The main aim of this study was to identify novel candidate genes and miRNAs that may contribute to the pathophysiology of hyperplastic AT. Therefore, wide gene and microRNA (miRNA) expression patterns were assessed in subcutaneous AT of 16 morbidly obese women before and after surgery-induced weight loss. Validation of microarray data was performed by quantitative real-time PCR both longitudinally (n=25 paired samples) and cross-sectionally (25 obese vs. 26 age-matched lean women). Analyses in macrophages and differentiated human adipocytes were also performed to try to comprehend the associations found in AT. 5,018 different probe sets identified significant variations in gene expression after treatment (adjusted p-value<0.05). A set of 16 miRNAs also showed significant modifications. Functional analysis revealed changes in genes and miRNAs associated with cell cycle, development and proliferation, lipid metabolism, and the inflammatory response. Canonical affected pathways included TREM1, PI3K, and EIF2 signaling, hepatic stellate cell activation, and mitochondrial function. Increased expression of SLC27A2, ELOVL6, FASN, GYS2, LGALS12, PKP2, ACLY, and miR-575, as well as decreased FOS, EGFL6, PRG4, AQP9, DUSP1, RGS1, EGR1, SPP1, LYZ, miR-130b, miR-221, and miR-155, were further validated. The clustering of similar expression patterns for gene products with related functions revealed molecular footprints, some of them described for the first time, which elucidate changes in biological processes after the surgery-induced weight loss.
Publication Title
Surgery-Induced Weight Loss Is Associated With the Downregulation of Genes Targeted by MicroRNAs in Adipose Tissue.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Arabidopsis thaliana
- 39 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
The Oscillation Zone (OZ) of unsynchronized roots was disected and divided into an upper (OZ2) and lower (OZ1) half .
Publication Title
Oscillating gene expression determines competence for periodic Arabidopsis root branching.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina humanRef-8 v2.0 expression beadchip
Description
The study was aimed at identifying genes directly or indirectly regulated by miR-205 in the prostate. To this purpose, DU145 prostate cancer cells, which express miR-205 at very low levels, were transfected with miR-205 synthetic precursor and consequent alterations of gene expression analyzed using a microarray approach.
Publication Title
miR-205 Exerts tumor-suppressive functions in human prostate through down-regulation of protein kinase Cepsilon.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
The myogenic regulatory factor MRF4 is expressed at high levels in myofibers of adult skeletal muscle, but its function is unknown. Here we show that knockdown of MRF4 in adult muscle causes hypertrophy and prevents denervation-induced atrophy. This effect is accompanied by increased protein synthesis and the widespread activation of genes involved in muscle contraction, excitation-contraction coupling and energy metabolism, many of which are known targets of MEF2 transcription factors. Genes regulated by MEF2 represent the top-ranking gene set enriched after Mrf4 RNAi, and a MEF2 reporter is inhibited by co-transfected MRF4 and activated by Mrf4 RNAi. The role of MEF2 in mediating the effect of MRF4 knockdown is supported by the finding that Mrf4 RNAi-dependent increase in fiber size is prevented by dominant negative MEF2, while constitutively active MEF2 is able to induce myofiber hypertrophy. The nuclear localization of the MEF2 co-repressor HDAC4 is impaired by Mrf4 knockdown, suggesting that MRF4 acts by stabilizing a repressor complex that controls MEF2 activity. The demonstration that fiber size in adult skeletal muscle is controlled by the MRF4-MEF2 axis opens new perspectives in the search for therapeutic targets to prevent muscle wasting, in particular sarcopenia and cachexia.
Publication Title
MRF4 negatively regulates adult skeletal muscle growth by repressing MEF2 activity.
Sample Metadata Fields
Specimen part
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