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GSE22298
Homo sapiens
15 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Targets of Retinoic Acid (RA) were identified in primary human epidermal keratinocytes grown in the presence or absence of all-trans retinoic acid for 1, 4, 24, 48 and 72 hours. Targets of Thyroid Hormone (T3) were identified in primary human epidermal keratinocytes grown in the presence or absence of the hormone; same controls as for RA.
Publication Title
Retinoid-responsive transcriptional changes in epidermal keratinocytes.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
The pigmented portion of ciliary epithelium in the adult mammalian eye harbors mitotically quiescent retinal sphere cells, which are capable of self-renewal and differentiating into retinal neurons when assayed in vitro; however, very little is known about the molecular mechanism controlling the proliferation and differentiation of these adult retinal stem cells or their molecular resemblance to mutipotent stem/progenitor cells during early eye development. This experiment studies the gene expression of first passage and primary human and mouse retinal sphere cells.
Publication Title
Recent developments in StemBase: a tool to study gene expression in human and murine stem cells.
Sample Metadata Fields
Sex
View Samples- Arabidopsis thaliana
- 12 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Two nuclear 5'-3' exonucleases XRN2/3 in Arabidopsis thaliana are homologs of the yeast and human Rat1/Xrn2, which are involved in degradation and processing of several classes of nuclear RNAs and in transcription termination of RNA polymerase II. Here we show that knockdown of XRN3 leads to altered expression of several hundred of the Arabidopsis genes and accumulation of new non-coding RNAs. Using strand-specific short read sequencing we reveal a widespread accumulation of intergenic transcripts in xrn3 mutants. These non-coding XAT (xrn3-associated transcripts) RNAs are generated by Pol II read-through transcription and are usually polyadenylated and lack the 5' cap structure. We show that XRN3-mediated changes in expression of a subset of genes are related to XAT transcription and may be enhanced by XAT-mRNA chimeras produced in xrn3 plants while antisense XATs may trigger siRNA production. Our results highlight the important role of the Rat1/Xrn2 5'-3' exoribonucleases in the torpedo mechanism of Pol II transcription termination and show that a global disturbance in this process significantly impacts both gene expression and transcriptome integrity.
Publication Title
Defective XRN3-mediated transcription termination in Arabidopsis affects the expression of protein-coding genes.
Sample Metadata Fields
Age, Specimen part, Time
View Samples- Mus musculus
- 11 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Transcriptome analysis of nucleus accumbens shell samples from RAR-null mutant mice and their wild type littermates
Publication Title
Genome-wide Analysis of RARβ Transcriptional Targets in Mouse Striatum Links Retinoic Acid Signaling with Huntington's Disease and Other Neurodegenerative Disorders.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 7 Downloadable Samples
Illumina HiSeq 2500
Description
Fragile X syndrome (FXS), the most common genetic form of intellectual disability in male, is caused by silencing of the FMR1 gene by hypermethylation of the CGG expansion mutation in the 5'UTR region of FMR1 in FXS patients. Here, we applied recently developed DNA methylation editing tools to reverse this hypermethylation event. Targeted demethylation of the CGG expansion by dCas9-Tet1/sgRNA switched the heterochromatin status of the upstream FMR1 promoter to an active chromatin state restoring a persistent expression of FMR1 in FXS iPSCs. Neurons derived from methylation edited FXS iPSCs rescued the electrophysiological abnormalities and restored a wild-type phenotype upon the mutant neurons. FMR1 expression in edited neurons was maintained in vivo after engrafting into the mouse brain. Finally, demethylation of the CGG repeats in post-mitotic FXS neurons also reactivated FMR1. Our data establish demethylation of the CGG expansion is sufficient for FMR1 reactivation, suggesting potential therapeutic strategies for FXS. Overall design: RNA-seq of FXS iPSC and neurons derived from FXS iPSC infected with lentiviruses expressing dCas9-Tet1-P2A-tBFP (dC-T) and a mCherry-expressing sgRNA targeting CGG repeats.
Publication Title
Rescue of Fragile X Syndrome Neurons by DNA Methylation Editing of the FMR1 Gene.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 28 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Differentiating human dendritic cells were stimulated for 12 hours with RXR agonists (LG268, 9CRA, R- and S-9CDHRA) or agonists for RXR partners including GW3965 (LXR/ panagonist), RSG (PPAR agonist), and GW1516 (PPAR agonist) and AM580 (RARa agonist). The gene expression changes were detected globally by Affymetrix Human Genome U133 Plus 2.0 Arrays.
Publication Title
9-cis-13,14-Dihydroretinoic Acid Is an Endogenous Retinoid Acting as RXR Ligand in Mice.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens, Rattus norvegicus
- 25 Downloadable Samples
Illumina HumanHT-12 V3.0 expression beadchip, Illumina Rat Ref-12 v1
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 25 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
With the population of older and overweight individuals on the rise in the Western world, there is an ever greater need to slow the aging processes and reduce the burden of age-associated chronic disease that would significantly improve the quality of human life and reduce economic costs. Caloric restriction (CR), is the most robust and reproducible intervention known to delay aging and to improve healthspan and lifespan across species (1); however, whether this intervention can extend lifespan in humans is still unknown. Here we report that rats and humans exhibit similar responses to long-term CR at both the physiological and molecular levels. CR induced broad phenotypic similarities in both species such as reduced body weight, reduced fat mass and increased the ratio of muscle to fat. Likewise, CR evoked similar species-independent responses in the transcriptional profiles of skeletal muscle. This common signature consisted of three key pathways typically associated with improved health and survival: IGF-1/insulin signaling, mitochondrial biogenesis and inflammation. To our knowledge, these are the first results to demonstrate that long-term CR induces a similar transcriptional profile in two very divergent species, suggesting that such similarities may also translate to lifespan-extending effects in humans as is known to occur in rodents. These findings provide insight into the shared molecular mechanisms elicited by CR and highlight promising pathways for therapeutic targets to combat age-related diseases and promote longevity in humans.
Publication Title
Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 32 Downloadable Samples
- Affymetrix Human Gene 1.1 ST Array (hugene11st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Gene 1.1 ST Array (hugene11st)
Description
Natural Killer (NK) cells present natural cytotoxicity against tumor cells, although their activity is increased after activation. NK cell activation depends on a complex intracellular signaling process mediated by activating and inhibitory receptors and the functional outcome depends on the integration of the activating and inhibitory signals received. Soluble cytokines and/or ligands on target cells bind the NK cell receptors, and hence, influence the final NK cell response: attack versus ignorance.
Publication Title
All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity.
Sample Metadata Fields
Specimen part, Subject
View Samples