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GSE84813
Homo sapiens
12 Downloadable Samples
Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
In order to explore the funciton of p53 splice variant in DNA damage response, we utilized CRISPR-cas9 genome editing technique to specifically knock out this variant in MCF7 cells.
Publication Title
Identification of a DNA Damage-Induced Alternative Splicing Pathway That Regulates p53 and Cellular Senescence Markers.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina HiSeq 2000
Description
Disruption of the MECP2 gene leads to Rett syndrome (RTT), a severe neurological disorder with features of autism. MECP2 encodes a methyl-DNA-binding protein that is proposed to function as a transcriptional repressor, but, despite numerous studies examining neuronal gene expression in MeCP2 mutants, no coherent model has emerged for how MeCP2 regulates transcription. Here we identify a genome-wide length-dependent increase in the expression of long genes in neurons lacking MeCP2. This gene misregulation occurs in human RTT brains and correlates with onset and severity of phenotypes in Mecp2 mutant mice, suggesting that the disruption of long gene expression contributes to RTT pathology. We present evidence that MeCP2 represses long genes by binding to brain-enriched, methylated CA dinucleotides within genes and show that loss of methylated CA in the brain recapitulates gene expression defects observed in MeCP2 mutants. We find that long genes encode proteins with neuronal functions, and overlap substantially with genes that have been implicated in autism and Fragile X syndrome. Reversing the overexpression of long genes in neurons lacking MeCP2 can improve some RTT-associated cellular deficits. These findings suggest that a function of MeCP2 in the mammalian brain is to temper the expression of genes in a length-dependent manner, and that mutations in MeCP2 and possibly other autism genes may cause neurological dysfunction by disrupting the expression of long genes in the brain. Overall design: Total RNA-seq Data from the visual cortex of wild-type and MeCP2 knockout animals at 8-10 weeks of age
Publication Title
Disruption of DNA-methylation-dependent long gene repression in Rett syndrome.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Changes in nuclear Ca2+ homeostasis activate specific gene expression programs and are central to the acquisition and the plastic storage of memories. DREAM /KChIP proteins form heterotetramers that bind DNA and repress transcription in a Ca2+-dependent manner. Single ablation of one member of the DREAM/KChIP family may result in a mild or the absence of phenotype due to partial gene compensation. To study the function of DREAM/KChIP proteins in the brain, we used transgenic mice expressing a Ca2+-insensitive/CREB-independent dominant active mutant DREAM (daDREAM). We show that daDREAM controls the expression of several activity-dependent transcription factors including Npas4, Nr4a1, Mef2C, JunB and c-Fos, as well as the chromatin modifying enzyme Mbd4 and proteins related to actin polymerization like Arc and gelsolin. Thus, directly or through these targets, expression of daDREAM in the forebrain resulted in a complex phenotype characterized by i) impaired learning and memory, ii) loss of recurrent inhibition and enhanced LTP in the dentate gyrus without affecting Kv4-mediated potassium currents, and iii) modified spine density in DG granule neurons. Our results propose DREAM as a master-switch transcription factor regulating several activity-dependent gene expression programs to control synaptic plasticity, learning and memory.
Publication Title
DREAM controls the on/off switch of specific activity-dependent transcription pathways.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
We compared gene expression profiles between asymptomatic and symptomatic atherosclerotic plaques from the same patient. This was accomplished by analyzing carotid plaques from four patients with bilateral high-grade carotid artery stenoses one being symptomatic (TIA or stroke) and the other asymptomatic.
Publication Title
Microarray analysis reveals overexpression of CD163 and HO-1 in symptomatic carotid plaques.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage, Subject, Time
View Samples- Mus musculus
- 14 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The aim of the experiment was to compare to single and combined effect of Ikaros activation and IL-7 withdrawal in the Ikaros-null pre-B cell line BH1
Publication Title
Ikaros is absolutely required for pre-B cell differentiation by attenuating IL-7 signals.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We have observed that follicular B cells from mice with a hypomorphic mutation (IkL/L) in the Ikzf1 gene (which encodes the Ikaros transcription factor) exhibit an increased proliferative response to anti-IgM stimulation (Kirstetter et al, Eur J Immunol, 32:720-30, 2002). We asked if Ikaros controls the transcriptional response that unfolds after activation, or if differences in the transcriptional landscape of resting B cells could explain the altered response. To this end, we have determined the transcriptome of unstimulated WT and IkL/L follicular B cells, as well as that of cells stimulated for 3h and 12h with anti-IgM. Samples from 2 independent experients were analyzed.
Publication Title
Ikaros limits follicular B cell activation by regulating B cell receptor signaling pathways.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Ikaros hypomorphic mice (IkL/L) show plasmacytoid dendritic cell (pDC) defects with an absence of pDCs in the peripheral organs and a reduction of pDCs in the bone marrow (BM). Moreover in vitro differentiation of pDC from IkL/L total BM cells is also defective.
Publication Title
Ikaros cooperates with Notch activation and antagonizes TGFβ signaling to promote pDC development.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To assess the importance of the Wnt pathway during T cell develoment, we generated a mouse line (R26-cat) in which high levels of active -catenin are maintained throughout T cell development. Young R26-cat mice (6-week-old) show a differentiation block at the CD4+CD8+ DP stage. All R26-cat mice develop T cell leukemias with a DP phenotype at 5-6 months of age.
Publication Title
β-Catenin activation synergizes with Pten loss and Myc overexpression in Notch-independent T-ALL.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 95 Downloadable Samples
- IlluminaHiSeq2500
Description
The purpose of current study is to identify the differentiated gene expression associated with mouse 11B3 deletion, syntenic to human chromosome 17p13.1. We compared four different mouse acute myeloid leukemia cells, freshly isolated from mouse bone marrows with either 11B3fl/p53fl;shNf1;shMll3;Vav1-Cre or p53fl/fl;shNf1;shMll3;Vav1-Cre. The RNA-seq results indicate that genes located on chromosome 11B3 mostly reduce gene expression level in 11B3 deleted leukemia cells. Overall design: Examination RNA expression level in 11B3-deleted vs p53-loss only samples.
Publication Title
Deletions linked to TP53 loss drive cancer through p53-independent mechanisms.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 42 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
In this survey we effectively combined transcriptomics, proteomics and targeted-metabolomics to analyse the temporal relationship of alterations in liver preceding and accompanying the development of HFD-mediated hepatic insulin resistance. To assess HFD-mediated alterations in physiological parameters, insulin sensitivity, and molecular adaptations in liver male C3HeB/FeJ mice treated with a high-fat diet (HFD) for 7, 14, or 21 days and compared to age- matched controls fed low-fat diet (LFD).
Publication Title
High fat diet-induced modifications in membrane lipid and mitochondrial-membrane protein signatures precede the development of hepatic insulin resistance in mice.
Sample Metadata Fields
Sex, Age, Treatment, Time
View Samples