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GSE4356
Mus musculus
27 Downloadable Samples
Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Deregulated expression of the Myc transcription factor is a frequent causal mutation in human cancer. Thousands of putative Myc target genes have been identified in in vitro studies, indicating that Myc exerts highly pleiotropic effects within cells and tissues. However, the complexity and diversity of Myc gene targets has confounded attempts at identifying which of these genes are the critical targets mediating Myc-driven tumorigenesis in vivo. Acute activation of Myc in a reversibly switchable transgenic model of Myc-mediated cell tumorigenesis induces rapid tumor onset whereas subsequent Myc de-activation triggers equally rapid tumor regression. Thus, sustained Myc activity is required for tumor maintenance. We have used this reversibly switchable kinetic tumor model in combination with high-density oligonucleotide microarrays to develop an unbiased strategy for identifying candidate Myc-regulated genes responsible for maintenance of Myc-dependent tumors. Consistent with known Myc functions, some Myc-regulated genes are involved in cell growth, cycle and proliferation. In addition, however, many Myc-regulated genes are specific to cells, indicating that a significant component of Myc action is cell-type specific. Finally, we identify a very restricted cadre of genes whose expression is inversely regulated upon Myc activation-induced tumor progression and de-activation-induced tumor regression. By definition, such genes are candidates for tumor maintenance functions. Combining reversibly switchable, transgenic models of tumor formation and regression with genomic profiling offers a novel strategy with which to deconvolute the complexities of oncogenic signaling pathways in vivo
Publication Title
Reversible kinetic analysis of Myc targets in vivo provides novel insights into Myc-mediated tumorigenesis.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 111 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Skeletal muscle atrophy is a consequence of many diseases, environmental insults, inactivity, age and injury. Atrophy is characterized by active degradation and removal of contractile proteins and a reduction in fiber size. Animal models have been extensively used to identify pathways leading to atrophic conditions. Here we have used genome-wide expression profiling analysis and quantitative PCR to identify the molecular changes that occur in two clinically relevant animal mouse models of muscle atrophy, hindlimb casting and Achilles tendon laceration (tenotomy). Gastrocnemius muscle samples were collected 2, 7 and 14 days after insult. The total amount of muscle loss as measured by wet weight and muscle fiber size was equivalent between models, although tenotomy resulted in a more rapid induction of muscle atrophy. Furthermore, tentomy resulted in the regulation of significantly more mRNA transcripts then casting. Analysis of the regulated genes and pathways suggest that the mechanism of atrophy is distinct between these models. The degradation following casting appears ubiquitin-proteasome-mediated while degradation following tenotomy appears lysosomal and matrix-metalloproteinase (MMP)-mediated. This data suggests that there are multiple mechanisms leading to muscle atrophy and that specific therapeutic agents may be necessary to combat the atrophy seen under different conditions.
Publication Title
Distinct protein degradation profiles are induced by different disuse models of skeletal muscle atrophy.
Sample Metadata Fields
Sex, Specimen part, Treatment, Time
View Samples- Homo sapiens
- 30 Downloadable Samples
NextSeq 500
Description
10X-based scRNA-seq data human fetal kidneys at 5 different ages Overall design: w9, w11, w13, w16 and w18 human fetal kidneys
Publication Title
Single-cell transcriptomics reveals gene expression dynamics of human fetal kidney development.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
We have generated stable human ESCs (H9) expressing control or DAP5-targeting shRNA. Polysome profiles reveal no major changes in overall translation. PolyA+ RNA and RNA accociated with heavy polysomal fractions were purified in biological duplicates and sequenced using Illumina HiSeq 2000 instrument. We identified 122 potential mRNA targets of DAP5 translation that display reduced ribosomal loading, and hence reduced translation, in the absence of DAP5. Overall design: Total mRNA and heavy polylsomal fractions from shNT and shDAP5 expressing hESCs, each in duplicate, was deep sequenced.
Publication Title
Cap-independent translation by DAP5 controls cell fate decisions in human embryonic stem cells.
Sample Metadata Fields
Subject
View Samples- Mus musculus, Homo sapiens
- 28 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
All highly and poorly permeable metastases from the same mouse brain were collected by laser capture microdissection. Total RNA from both metastatic lesions and immediate microenvironment was isolated from 5 mice bearing 231-BR metastases. As control 4 healthy mouse brains were included.
Publication Title
Reactive astrocytic S1P3 signaling modulates the blood-tumor barrier in brain metastases.
Sample Metadata Fields
Subject
View Samples- Sus scrofa
- 30 Downloadable Samples
- Affymetrix Porcine Genome Array (porcine)
Description
Background: Cerebral ischemia/reperfusion injury is a common secondary effect of cardiac arrest which is largely responsible for postresuscitative mortality. Therefore development of therapies which restore and protect the brain function after cardiac arrest is essential. Methylene blue (MB) has been experimentally proven neuroprotective in a porcine model of global ischemia-reperfusion in experimental cardiac arrest. However, no comprehensive analyses have been conducted at gene expression level.
Publication Title
Immunoproteasomes preserve protein homeostasis upon interferon-induced oxidative stress.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
RNAseq analysis of YAP and Myc induced in quiescent and confluent 3T9 fibroblasts Overall design: RNAseq analysis of YAP and Myc induced in quiescent and confluent 3T9 fibroblasts
Publication Title
Transcriptional integration of mitogenic and mechanical signals by Myc and YAP.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The ubiquitin proteasome system (UPS) is known to possess important regulatory functions in the immune response. To gain a better and first comprehensive insight into the mechanisms of remodelling of UPS related gene expression inresponse to interferon-gamma, we undertook a comparative gene expression profiling during interferon-gamma stimulation at very early time points.
Publication Title
Immunoproteasomes preserve protein homeostasis upon interferon-induced oxidative stress.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 192 Downloadable Samples
- NextSeq500
Description
A cell supsension containing an equal mix of HEK and 3T3 cells was used in the Fluidigm C1 Overall design: Suspensions of 3T3 and HEK cells were diluted down to a concentration of 250,000 per mL and mixed 1:1, then loaded onto two medium C1 cell capture chips.
Publication Title
Highly Parallel Genome-wide Expression Profiling of Individual Cells Using Nanoliter Droplets.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 43 Downloadable Samples
- Illumina HiSeq 2000
Description
Tumors driven by activation of the transcription factor Myc generally show oncogene addiction. However, the gene-expression programs that depend upon sustained Myc activity in those tumors remain unknown. We have addressed this issue in a model of liver carcinoma driven by a reversible tet-Myc transgene, combining gene expression profiling with the mapping of Myc and RNA Polymerase II on chromatin. Switching off the oncogene in advanced carcinomas revealed that Myc is required for the continuous activation and repression of distinct sets of genes, constituting no more than half of those deregulated during tumor progression, and an even smaller subset of all Myc-bound genes. We further showed that a Myc mutant unable to associate with the co-repressor protein Miz1 is defective in the initiation of liver tumorigenesis. Altogether, our data provide the first detailed analysis of a Myc-dependent transcriptional program in a fully developed carcinoma, revealing that the critical effectors of Myc in tumor maintenance must be included within defined subsets (ca. 1,300 each) of activated and repressed genes. Overall design: RNAseq samples of control liver (n=11), tet-Myc tumors (n=16), tet-Myc tumors with short-term Myc inactivation (n=8), tet-MycVD tumors (n=11)
Publication Title
Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples