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SRP150775
Mus musculus
2 Downloadable Samples
Illumina HiSeq 2500
Description
Intestinal organoids are complex three-dimensional structures that mimic cell type composition and tissue organization of the intestine by recapitulating the self-organizing capacity of cell populations derived from a single stem cell. Crucial in this process is a first symmetry-breaking event, in which only a fraction of identical cells in a symmetrical cyst differentiate into Paneth cells, which in turn generates the stem cell niche and leads to asymmetric structures such as crypts and villi. We here combine a quantitative single-cell gene expression and imaging approach to characterize the development of intestinal organoids from a single cell. We show that intestinal organoid development follows a regeneration process driven by transient Yap1 activation. Cell-to-cell variability in Yap1, emerging in symmetrical cysts, initiates a Notch/Dll1 lateral inhibition event driving the symmetry-breaking event and the formation of the first Paneth cell. Our findings reveal how single cells exposed to a uniform growth-promoting environment have the intrinsic ability to generate emergent, self-organized behavior resulting in the formation of complex multicellular asymmetric structures. Overall design: Single cell RNA sequencing of single cells isolated from intestinal organoids day3 and intestinal organoids day 5
Publication Title
Self-organization and symmetry breaking in intestinal organoid development.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
Dysregulation of professional APC has been postulated as a major mechanism underlying Ag-specific T cell hyporesponsiveness in patients with patent filarial infection. To address the nature of this dysregulation, dendritic cells (DC) and macrophages generated from elutriated monocytes were exposed to live microfilariae (mf), the parasite stage that circulates in blood and is responsible for most immune dysregulation in filarial infections. DC exposed to mf for 2496 h showed a marked increase in cell death and caspase-positive cells compared with unexposed DC, while mf exposure did not induce apoptosis in macrophages. Interestingly, 48 h exposure of DC to mf induced mRNA expression of the pro-apoptotic gene TRAIL and both mRNA and protein expression of TNF-alpha. mAb to TRAIL-R2, TNF-R1, or TNF-alpha partially reversed mf-induced cell death in DC, as did knocking down the receptor for TRAIL-R2 using small interfering RNA. Mf also induced gene expression of BH3-interacting domain death agonist (Bid) and protein expression of cytochrome c in DC; mf-induced cleavage of Bid could be shown to induce release of cytochrome c, leading to activation of caspase 9. Our data suggest that mf induce DC apoptosis in a TRAIL- and TNF-alpha-dependent fashion.
Publication Title
Induction of TRAIL- and TNF-alpha-dependent apoptosis in human monocyte-derived dendritic cells by microfilariae of Brugia malayi.
Sample Metadata Fields
Sex, Treatment, Race
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We sought to examine the mechanism through which phospho-mutants can contribute to the transformation of MCF10A acini. To investigate this, we examined the RNA abundance of Myc and Myc phospho-mutants (T58A, S71A/S81A, and Myc-4A) against a GFP control.
Publication Title
MYC phosphorylation at novel regulatory regions suppresses transforming activity.
Sample Metadata Fields
Cell line
View Samples- Mus musculus, Rattus norvegicus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 4 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Determination of the mechanism by which fibrinogen, a central blood coagulation protein drives immunological responses targeted to the CNS. Results identify the factors involved in the regulation and provide mechanistic basis.
Publication Title
Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Determination of the mechanism by which fibrinogen, a central blood coagulation protein drives immunological responses targeted to the CNS. Results identify the factors involved in the regulation and provide mechanistic basis.
Publication Title
Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 18 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
The purpose of the dataset is to analyze expression of genes induced by KRAS and regulated by TBK1
Publication Title
Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 31 Downloadable Samples
- Illumina HiSeq 2500
Description
DNA methylation and other repressive epigenetic marks are erased genome-wide in mammalian primordial germ cells (PGCs), the early embryo and in naïve embryonic stem cells (ESCs). This is a critical phase for transposon element (TE) defense since presumably alternative pathways need to be employed to limit their activity. It has been reported that pervasive transcription is enriched for TEs in ESCs in comparison to somatic cells. Here we test the hypothesis that pervasive transcription overlapping TEs forms a sensor for loss of their transcriptional repression. Overlapping sense and antisense transcription is found in TEs, and the increase of sense transcription induced by acute deletion of DNMT1 leads to the emergence of small RNAs. These small RNAs are loaded into ARGONAUTE 2 suggesting an endosiRNA mechanism for transposon silencing. Indeed, deletion of DICER reveals this mechanism to be important for silencing of certain transposon classes, while others are additionally repressed by deposition of repressive histone marks. Our observations suggest that pervasive transcription overlapping with TEs resulting in endosiRNAs is a transposon sensor that restrains their activity during epigenetic reprogramming in the germline. Overall design: Total RNA-seq libraires (2 biological replicates of 16 samples, 1 biological replicate of 1 sample)
Publication Title
An endosiRNA-Based Repression Mechanism Counteracts Transposon Activation during Global DNA Demethylation in Embryonic Stem Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus, Homo sapiens
- 5 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Hypomethylation of the IL17RC promoter associates with age-related macular degeneration.
Sample Metadata Fields
Age, Specimen part, Disease, Cell line
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Age related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly population worldwide. While recent studies have demonstrated strong genetic associations of single nucleotide polymorphisms within a number of genes and AMD, other modes of regulation are also likely to play a role in its aetiology. We undertook DNA methylation microarray analysis on monozygotic and dizygotic twins who were discordant for AMD and identified methylated IL17RC promoters as being present only in non-AMD control individuals rather than in AMD patients. We validated this finding of a significantly decreased level of methylation on the IL17RC promoter in AMD siblings as well as in a case control study involving 202 genetically unrelated AMD patients and 96 controls (95% CI, 0.03-0.17, P=3.1x10-8). Further, we showed that hypomethylation of the IL17RC promoter in AMD patients led to an elevated expression of its protein and mRNA in peripheral blood as well as in the retina and choroid, suggesting that the DNA methylation pattern and expression of IL17RC may potentially serve as a biomarker for the diagnosis of AMD and likely plays a role in disease pathogenesis.
Publication Title
Hypomethylation of the IL17RC promoter associates with age-related macular degeneration.
Sample Metadata Fields
Specimen part, Cell line
View Samples