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GSE23547
Mus musculus
7 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
In order to investigate what signalling pathways are turned on by tenascin-C, we generated Mouse Embryonic Fibroblasts (MEFs) deficient for tenascin-C and compared their gene expression profile to MEFs proficient for tenascin-C.
Publication Title
Tenascin-C triggers fibrin accumulation by downregulation of tissue plasminogen activator.
Sample Metadata Fields
Specimen part
View Samples- Staphylococcus aureus
- 15 Downloadable Samples
- Affymetrix S. aureus Genome Array (saureus)
Description
In the present study, we employed Affymetrix Staphylococcus aureus GeneChip arrays to investigate the dynamics of global gene expression profiles during the cellular response of Staphylococcus aureus to Ortho-Phenylphenol, which involved initial growth inhibition and metabolism.
Publication Title
Microarray analysis of toxicogenomic effects of ortho-phenylphenol in Staphylococcus aureus.
Sample Metadata Fields
No sample metadata fields
View Samples- Staphylococcus aureus
- 15 Downloadable Samples
- Affymetrix S. aureus Genome Array (saureus)
Description
In the present study, we employed Affymetrix Staphylococcus aureus GeneChip arrays to investigate the dynamics of global gene expression profiles during the cellular response of Staphylococcus aureus to triclosan, which involved initial growth inhibition and metabolism.
Publication Title
Microarray analysis of toxicogenomic effects of triclosan on Staphylococcus aureus.
Sample Metadata Fields
No sample metadata fields
View Samples- Pseudomonas aeruginosa
- 12 Downloadable Samples
- Affymetrix Pseudomonas aeruginosa Array (paeg1a)
Description
In the present study, we employed Affymetrix Pseudomonas aeruginosa GeneChip arrays to investigate the dynamics of global gene expression profiles during the cellular response of Pseudomonas aeruginosa to ortho-phenylphenol, which involved initial growth inhibition and metabolism.
Publication Title
Toxicogenomic response of Pseudomonas aeruginosa to ortho-phenylphenol.
Sample Metadata Fields
No sample metadata fields
View Samples- Pseudomonas aeruginosa
- 9 Downloadable Samples
- Affymetrix Pseudomonas aeruginosa Array (paeg1a)
Description
In the present study, we employed Affymetrix Pseudomonas aeruginosa GeneChip arrays to investigate the dynamics of global gene expression profiles during the cellular response of Pseudomonas aeruginosa to Chlorhexidine diacetate, which involved initial growth inhibition and metabolism.
Publication Title
Global transcriptomic response of Pseudomonas aeruginosa to chlorhexidine diacetate.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 48 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The liver circadian clock is reprogrammed by nutritional challenge through the rewiring of specific transcriptional pathways. As the gut microbiota is tightly connected to host metabolism, whose coordination is governed by the circadian clock, we explored whether gut microbes influence circadian homeostasis and how they distally control the peripheral clock in the liver. Using fecal transplant procedures we reveal that, in response to high fat diet, the gut microbiota drives PPAR-mediated activation of newly oscillatory transcriptional programs in the liver. Moreover, antibiotics treatment prevents PPAR-driven transcription in the liver, underscoring the essential role of gut microbes in clock reprogramming and hepatic circadian homeostasis. Thus, a specific molecular signature characterizes the influence of the gut microbiome in the liver, leading to the transcriptional rewiring of hepatic metabolism.
Publication Title
Gut microbiota directs PPARγ-driven reprogramming of the liver circadian clock by nutritional challenge.
Sample Metadata Fields
Specimen part
View Samples- Arabidopsis thaliana
- 6 Downloadable Samples
Illumina HiSeq 1500
Description
The goal of this study was to compare the transcriptional profile (RNA-seq) of imbibed Arabidopsis thaliana Columbia-0 ecotype seeds that were treated with a 20 min red or far red pulse. The red-light pulse induces germination. Overall design: Col-0 seeds were sown in clear plastic boxes, each containing 10 mL of 0.8 % (w/v) agar in demineralized water. To establish a minimum and equal photo-equilibrium, seeds were imbibed for 2 hours in darkness and then irradiated for 20 min with a saturated far-red pulse (FRp, calculated Pfr/P= 0.03, 42 µmol.m-2.s-1) in order to minimize the quantities of Pfr formed during their development in the mother plant. Seeds were then stratified at 5 °C in darkness for 3 days, prior to the 20 minutes with a saturated red pulse (Rp, calculated Pfr/P= 0.87, 0.05 µmol.m-2.s-1) or FRp. Three biological replicates of each condition were collected 12 hours after the corresponding R and FR light pulses.
Publication Title
Alternative Splicing Regulation During Light-Induced Germination of <i>Arabidopsis thaliana</i> Seeds.
Sample Metadata Fields
Subject
View Samples- Mus musculus
- 72 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The circadian clock orchestrates rhythms in physiology and behavior, allowing the organism to adapt to daily environmental changes. Recently, efforts have been made to unravel the connection between the circadian clock and metabolism and to understand how the peripheral clock in different organs coordinates circadian responses to maintain metabolic homeostasis. It is becoming clear that diet can influence diurnal rhythms, however, the molecular mechanisms responsible for alterations in daily oscillations and how tissue-specific clocks interpret a nutritional challenge are not well understood. Here, we reveal tissue-specific circadian plasticity in response to a ketogenic diet (KD) in both the liver and intestine and a remarkable deviation within these two tissues following subsequent carbohydrate supplementation. KD caused a dramatic change in the circadian transcriptome in both liver and intestine in a tissue-specific fashion. In particular, both the amplitude of clock genes as well as specific BMAL1 recruitment was profoundly altered by KD while the intestinal clock was devoid of such plasticity. While PPARG nuclear accumulation was circadian in both tissues, it showed substantial phase specificity as did downstream targets. Finally, the gut and liver clocks had distinct responses to carbohydrate supplementation to KD composition, suggesting a higher plasticity in the ileum whose gene expression was almost restored to control baseline. For the first time our results demonstrate how nutrients modulate clock function in a tissue-specific manner, suggesting that a food stress arouses unique circadian molecular signatures in distinct peripheral tissues.
Publication Title
Distinct Circadian Signatures in Liver and Gut Clocks Revealed by Ketogenic Diet.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 27 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Global gene expression profiling of human iPSC and the iPSC-derived presomitic mesoderm(PSM), somite(SM), and the derivatives, dermomyotome(DM), dermatome(D), myotome(MYO), sclerotome(SCL) and syndetome(SYN).
Publication Title
Modeling human somite development and fibrodysplasia ossificans progressiva with induced pluripotent stem cells.
Sample Metadata Fields
Specimen part, Time
View Samples- Mus musculus
- 19 Downloadable Samples
- IlluminaHiSeq2500
Description
TET proteins oxidize 5-methylcytosine to 5-hydroxymethylcytosine and further oxidation products in DNA. Here we report that simultaneous deletion of Tet2 and Tet3 in mouse double-positive thymocytes resulted in dysregulated development and proliferation of invariant natural killer T (iNKT) cells. Tet2-Tet3-double-deficient (DKO) iNKT cells displayed pronounced skewing towards the NKT17 lineage, with increased DNA methylation and impaired expression of genes encoding the key lineage-specifying factors T-bet and ThPOK. Transfer of purified Tet2-Tet3 DKO iNKT cells into immunocompetent recipient mice resulted in uncontrolled expansion dependent on the nonclassical MHC protein CD1d, which presents lipid antigens to iNKT cells. Our data indicate that TET proteins regulate iNKT cell fate by ensuring proper development and maturation and suppressing aberrant T cell antigen receptor (TCR)-mediated proliferation. Overall design: DKO vs. wild type
Publication Title
TET proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells.
Sample Metadata Fields
No sample metadata fields
View Samples