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SRP196721
Homo sapiens
4 Downloadable Samples
Illumina HiSeq 2500
Description
With a model mimicking GBM tumor cell dispersal, transcriptome changes between core (immotile) and dispersive (motile) cells were analyzed. Many genes are differentially expressed between these populations. This study focused on the genes that are significantly upregulated in dispersive cells. Besides gene sets related with the cell cycle and cell survival, epithelial to mesenchymal transition gene set is upregulated in dispersive cells. In this gene set, this study identified SERPINE1 gene as an important regulator of GBM cell dispersal. Overall design: Examination of core and dispersive populations' transcriptome during U373 cell spheroid dispersal. 2 sets of samples were prepared each for core and dispersive cells.
Publication Title
Identification of <i>SERPINE1</i> as a Regulator of Glioblastoma Cell Dispersal with Transcriptome Profiling.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
The conditioned media from Bifidobacterium infantis (BCM) and Lactobacillus acidophilus (LCM) were reported to promote maturation of innate immune response gene expression, which explained the protective effects of probiotics in clinical necrotizing enterocolitis. We used microarray analysis to investigate the expression of genes involved in regulation of BCM and LCM in IL-1 stimulated immature human enterocytes.
Publication Title
Secreted Metabolites of Bifidobacterium infantis and Lactobacillus acidophilus Protect Immature Human Enterocytes from IL-1β-Induced Inflammation: A Transcription Profiling Analysis.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
Chromatin in eukaryotic nuclei is organized at multiple scales, from individual nucleosomes to specific loops between regulatory sequences, to the folding of large genomic regions into topological domains and segregation of whole chromosomes into territories. Many of the chromatin proteins that regulate this architecture, including the essential Polycomb Group (PcG) proteins, are themselves organized into subnuclear structures. Deciphering mechanistic links between protein organization and genome architecture requires precise description and mechanistic perturbations of both. Using super-resolution microscopy, we characterized the nanoscale organization of PcG proteins in Drosophila cells and find hundreds of small protein clusters, distinct from the large PcG bodies present in just a few copies per cell that have been the focus of previous investigations. We manipulated PcG clusters either by disrupting the polymerization activity of the conserved Sterile Alpha Motif (SAM) of the PcG protein Polyhomeotic (Ph) or increasing Ph levels in Drosophila S2 cells. Disrupting clustering using Ph SAM mutations disrupts chromatin interactions on scales from 50kb to 13Mb while increasing Ph levels increases both cluster number and long range chromatin interactions. RNA-seq and qPCR indicate that both perturbations also alter expression levels of many genes. Molecular simulations suggest a model in which PcG cluster formation on chromatin is governed by the kinetics of association between Ph SAMs and PcG cluster size is bounded by the affinity and occupancy of chromatin binding sites. Our results suggest that nanoscale organization of PcG proteins into small, abundant clusters on chromatin through the polymerization activity of Ph SAM shapes genome architecture by mediating numerous long-range chromatin interactions. Overall design: Two biological replicates of three RNA-seq samples from S2 cells, cells overexpresing wild-type Ph, and cells overexpressing polymerization defective Ph-ML
Publication Title
Chromatin topology is coupled to Polycomb group protein subnuclear organization.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 60 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 33 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.
Publication Title
A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.
Publication Title
A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.
Publication Title
A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The transcription factor FoxP3 partakes dominantly in the specification and function of FoxP3+ CD4+ T regulatory cells (Tregs), but is neither strictly necessary nor sufficient to determine the characteristic Treg transcriptional signature. Computational network inference and experimental testing assessed the contribution of several other transcription factors (TFs). Enforced expression of Helios or Xbp1 elicited specific signatures, but Eos, Irf4, Satb1, Lef1 and Gata1 elicited exactly the same outcome, synergizing with FoxP3 to activate most of the Treg signature, including key TFs, and enhancing FoxP3 occupancy at its genomic targets. Conversely, the Treg signature was robust to inactivation of any single cofactor. A redundant genetic switch thus locks-in the Treg phenotype, a model which accounts for several aspects of Treg physiology, differentiation and stability.
Publication Title
A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
MicroRNAs as modulators of smoking-induced gene expression changes in human airway epithelium.
Sample Metadata Fields
Sex, Age, Race
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
mRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy from healthy current and never smoker volunteers in order to determine relationships between microRNA and mRNA expression in bronchial epithelial cell samples across current and never smokers and within the same individual.
Publication Title
MicroRNAs as modulators of smoking-induced gene expression changes in human airway epithelium.
Sample Metadata Fields
Sex, Age, Race
View Samples