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GSE37935
Homo sapiens
6 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Sp1 is a transcription factor able to regulate many genes through its DNA binding domain, containing three zinc fingers. We were interested in identifying target genes regulated by Sp1, with a special emphasis to those involved in proliferation and cancer. Our approach was to treat HeLa cells with a siRNA directed against Sp1 mRNA (siSp1) to decrease the expression of Sp1 and, in turn, the genes activated by this transcription factor. Sp1 siRNA treatment led to a great number of differentially expressed genes as determined by whole genome cDNA microarray analysis. Underexpressed genes were selected since they represent putative genes activated by Sp1. These underexpressed genes were classified in six Gene Onthology categories, namely proliferation and cancer, mRNA processing, lipidic metabolism, glucidic metabolism, transcription and translation. Putative Sp1 binding sites were found in the promoters of the selected genes using the MatchTM software. After literature mining, 11 genes were selected for further validation of their expression levels using RT-real time PCR. Underexpression was confirmed for the 11 genes plus Sp1 in HeLa cells after siSp1 treatment. Additionally, EMSA and chromatin immunoprecipitation assays were performed to test for binding between Sp1 and the promoters of these genes. We observed binding of Sp1 to the promoters of RAB20, FGF21, IHPK2, ARHGAP18, NPM3, SRSF7, CALM3, PGD and Sp1 itself. Finally, the mRNA levels of RAB20, FGF21 and IHPK2, three genes related with proliferation and cancer, were determined after overexpression of Sp1 in HeLa cells, to confirm their relationship with Sp1.
Publication Title
Identification of novel Sp1 targets involved in proliferation and cancer by functional genomics.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina HiSeq 2000
Description
Epigenetic control of neural stem/progenitor cell fate is fundamental to achieve a fully brain architecture. Two intrinsic programs regulate neurogenesis, one by epigenetic-mediated gene transcription and another by cell cycle control. Whether and how these two are coordinated to determine temporally and spatially neural development remains unknown. Here we show that deletion of Trrap (Transcription translation associated protein), an essential cofactor for HAT (histone acetyltransferase), leads to severe brain atrophy due to a combination of cell death and a blockade of neuron production. Specifically, Trrap deletion forces differentiation of apical progenitor (AP) fate into basal progenitors (BP) and neurons thereby limiting the total neurogenic production. Despite Trrap’s general role in transcriptional regulation, a genome-wide transcriptome analysis of neuroprogenitors identified the cell cycle regulators that are specifically affected by Trrap deletion. Furthermore, E2F-dependent recruitment of HAT and transcription factors to the promoter of cell cycle regulators is impaired in Trrap-deleted neuroprogenitors. Consistent with these molecular changes, Trrap deletion lengthens particularly G1 and S phases in APs in vivo. Therefore, our study reveals an essential and a distinct function of Trrap-HAT in regulation of cell cycle progression that is required for proper determination of neuroprogenitor fate. Overall design: Determine gene transcriptions by comparing Trrap-deleted and wild type samples
Publication Title
Trrap-dependent histone acetylation specifically regulates cell-cycle gene transcription to control neural progenitor fate decisions.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2500
Description
We profiled the gene expression/splicing program of normal and hnRNP U-deficient mouse hearts by RNA-seq. Overall design: RNA-seq profiles of control and Hnrnpu mutant hearts at postnatal day 14. Hnrnpu mutant hearts were generated by breeding the Hnrnpu conditional knockout mice with Ckmm-Cre transgenic mice.
Publication Title
hnRNP U protein is required for normal pre-mRNA splicing and postnatal heart development and function.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 20 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset neuromuscular disorder characterized by the selective degeneration of upper and lower motor neurons, progressive muscle wasting and paralysis. To define the full set of alterations in gene expression in skeletal muscle during the course of the disease, we performed high-density oligonucleotide microarray analysis of gene expression in hind limb skeletal muscles of sod1(G86R) mice, one of the existing transgenic models of ALS. To monitor denervation-dependent gene expression, we determined the effects of short-term acute denervation on the muscle transcriptome after sciatic nerve axotomy.
Publication Title
Gene profiling of skeletal muscle in an amyotrophic lateral sclerosis mouse model.
Sample Metadata Fields
Sex, Age, Specimen part, Disease, Disease stage, Treatment, Subject, Time
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Expression of germ cell nuclear factor (GCNF, Nr6a1), an orphan member of the nuclear receptor gene family of transcription factors, during gastrulation and neurulation is critical for normal embryogenesis in mice. Gcnf represses the expression of the POU domain transcription factor Oct4 (Pou5f1) during mouse post-implantation development. Although Gcnf expression is not critical for the embryonic segregation of the germ cell lineage, we found that sexually dimorphic expression of Gcnf in germ cells correlates with the expression of pluripotency-associated genes, such as Oct4, Sox2, and Nanog, as well as the early meiotic marker gene Stra8. To elucidate the role of Gcnf during mouse germ cell differentiation, we generated an ex vivo Gcnf-knockdown model in combination with a regulated CreLox mutation of Gcnf. Lack of Gcnf impairs normal spermatogenesis and oogenesis in vivo, as well as the derivation of germ cells from embryonic stem cells (ESCs) in vitro. Inactivation of the Gcnf gene in vivo leads to loss of repression of Oct4 expression in both male and female gonads.
Publication Title
Germ cell nuclear factor regulates gametogenesis in developing gonads.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Cystatin D (CST5) is an inhibitor of several proteases of the cathepsin family that inhibits cell proliferation, migration and invasion of colon carcinoma cells. Some of these effects are unrelated to its antiprotease activity. Here, we use genome-wide expression microarrays to show that cystatin D regulates gene expression (including that of genes encoding transcription factors such as RUNX1, RUNX2, or MEF2C) in HCT116 cells.
Publication Title
Cystatin D locates in the nucleus at sites of active transcription and modulates gene and protein expression.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 74 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Background: There is limited data on how different RSV genotypes and associated viral loads influence disease phenotypes. We characterized the genetic variability of RSV strains during five non-consecutive respiratory seasons, and evaluated the role of RSV subtypes, genotypes and viral loads on clinical disease severity.
Publication Title
Respiratory Syncytial Virus Genotypes, Host Immune Profiles, and Disease Severity in Young Children Hospitalized With Bronchiolitis.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 59 Downloadable Samples
- Illumina Genome Analyzer II, Illumina Genome Analyzer IIx
Description
Amyotrophic Lateral Sclerosis (ALS) results from the selective and progressive degeneration of motor neurons. Although the underlying disease mechanisms remain unknown, glial cells have been implicated in ALS disease progression. Here we examine the effects of glial cell/motor neuron interactions on gene expression, using the hSOD1G93A mouse model of ALS. We detect striking cell autonomous and non-autonomous changes in gene expression in co-cultured motor neurons and glia, revealing that the two cell types profoundly affect each other. In addition, we found a remarkable concordance between the cell culture data, expression profiles of whole spinal cords, and of acutely isolated spinal cord cells, during disease progression in the G93A mouse model, providing validation of the cell culture approach. Bioinformatics analyses identified changes in the expression of specific genes and signaling pathways that may contribute to motor neuron degeneration in ALS, among which are TGF-b signaling pathways. Overall design: RNA-seq profiles of: 1) 43 Sandwich culture samples at 3 different time points (3, 7 and 14 days), in duplicate, in different combinations of genetic background WT/SOD1_G93A mutant glia and WT/SOD1_G93A mutant neurons; 2) 16 spinal cord samples at 4 different time points, WT and SOD1_G93A mutant.
Publication Title
Intricate interplay between astrocytes and motor neurons in ALS.
Sample Metadata Fields
Sex, Subject, Time
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Conrad et al. Nature 456, 344349 (2008) have generated human adult germline stem cells (haGSCs) from human testicular tissue, which they claim have similar pluripotent properties to human embryonic stem cells (hESCs). Here we investigate the pluripotency of haGSCs by using global gene-expression analysis based on their gene array data and comparing the expression of pluripotency marker genes in haGSCs and hESCs, and in haGSCs and human fibroblast samples derived from different laboratories, including our own. We find that haGSCs and fibroblasts have a similar gene-expression profile, but that haGSCs and hESCs do not. The pluripotency of Conrad and colleagues haGSCs is therefore called into question.
Publication Title
Human adult germline stem cells in question.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 42 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Pluripotency is the differentiation capacity of particular cells exhibited in the early embryo in vivo and embryonic stem (ES) cells have been shown to originate from the inner cell mass (ICM) of an E3.5 blastocyst. Although the potential for ES cells to differentiate into the three germ layers is equated to ICM cells, they differ in the ability to maintain the capacity for self-renewal. Despite several studies on the maintenance of ES cells in the ground state of pluripotency, the precise mechanism of conversion from the ICM to the ES cell remains unclear. Here , we have examined the cell characteristics and expression profile within the intermediate stages of ES cell derivation from the ICM. Gene clustering and ontology (GO) analyses showed a significant change in the expression of epigenetic modifiers and DNA methylation-related genes in the intermediate stages. We have proposed that an epithelial-to-mesenchymal transition (EMT) blockage is required during derivation of mouse ES cells from E3.5 blastocysts. This study suggests a novel mechanistic insight into ES cell derivation and provides a time-course transcriptome profiling resource for the dissection of gene regulatory networks that underlie the transition from ICM to ES cells.
Publication Title
Blockage of the Epithelial-to-Mesenchymal Transition Is Required for Embryonic Stem Cell Derivation.
Sample Metadata Fields
No sample metadata fields
View Samples