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Homo sapiens
20 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Melanomas are often infiltrated by activated inflammatory cells. Thus, melanoma cells are very likely stimulated by inflammatory cytokines.
Publication Title
Interleukins 1alpha and 1beta secreted by some melanoma cell lines strongly reduce expression of MITF-M and melanocyte differentiation antigens.
Sample Metadata Fields
Cell line
View Samples- Arabidopsis thaliana
- 27 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The transcription factor ABI4 Is required for the ascorbic acid-dependent regulation of growth and regulation of jasmonate-dependent defense signaling pathways in Arabidopsis.
Sample Metadata Fields
Age, Specimen part
View Samples- Arabidopsis thaliana
- 17 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
The role of abscisic acid (ABA) signalling in the ascorbic acid (AA)-dependent control of plant growth and defence was determined using the vtc1 and vtc2 mutants, which have impaired ascorbic acid synthesis, and in the abi4 mutant that is impaired in ABA-signalling. ABA levels were increase in the mutants relative to the wild type (Col0). Like vtc1 the vtc2 mutants have a slow growth relative to Col0. However, the wild type phenotype is restored in the abi4vtc2 double mutant. Similarly, the sugar sensing phenotype of in the abi4 is reversed in the abi4vtc2 double mutant. The vtc1 and vtc2 leaf transcriptomes show up to 70 % homology with abi4. Of the transcripts that are altered in the mutants a relative to Col0, only a small number are reversed in the abi4vtc2 double mutants relative to either abi4 or vtc2. We conclude that AA controls growth via an ABA and abi4-dependent signalling pathway. The vtc and abi4 mutants have enhanced glutathione levels and common redox signalling pathways leading to similar gene expression patterns.
Publication Title
The transcription factor ABI4 Is required for the ascorbic acid-dependent regulation of growth and regulation of jasmonate-dependent defense signaling pathways in Arabidopsis.
Sample Metadata Fields
Age, Specimen part
View Samples- Arabidopsis thaliana
- 10 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
The role of abscisic acid (ABA) signalling in the ascorbic acid (AA)-dependent control of plant growth and defence was determined using the vtc1 and vtc2 mutants, which have impaired ascorbic acid synthesis, and in the abi4 mutant that is impaired in ABA-signalling. ABA levels were increase in the mutants relative to the wild type (Col0). Like vtc1 the vtc2 mutants have a slow growth relative to Col0. However, the wild type phenotype is restored in the abi4vtc2 double mutant. Similarly, the sugar sensing phenotype of in the abi4 is reversed in the abi4vtc2 double mutant. The vtc1 and vtc2 leaf transcriptomes show up to 70 % homology with abi4. Of the transcripts that are altered in the mutants a relative to Col0, only a small number are reversed in the abi4vtc2 double mutants relative to either abi4 or vtc2. We conclude that AA controls growth via an ABA and abi4-dependent signalling pathway. The vtc and abi4 mutants have enhanced glutathione levels and common redox signalling pathways leading to similar gene expression patterns.
Publication Title
The transcription factor ABI4 Is required for the ascorbic acid-dependent regulation of growth and regulation of jasmonate-dependent defense signaling pathways in Arabidopsis.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 73 Downloadable Samples
Illumina HiSeq 2000
Description
Determination of the genes regulated by ERRalpha nuclear receptor in MDA-MB231 cells Overall design: MDA-MB231 cells were inactivated for ERRalpha using siRNA. Three different siRNAs were used (siE1, siE2, siE3). Cells treated with a control siRNA (siC samples) were used for comparison. Duplicate samples were analyzed. Transcriptomic analysis was performed by RNA-Seq
Publication Title
ERRα induces H3K9 demethylation by LSD1 to promote cell invasion.
Sample Metadata Fields
Cell line, Subject
View Samples
SRP043217- Homo sapiens
- 57 Downloadable Samples
- IlluminaHiSeq2000
Description
Determination of the genes regulated by LSD1 in MDA-MB231 cells Overall design: MDA-MB231 cells were inactivated for LSD1 using siRNA. Two different siRNAs were used (siL1, siL2). Cells treated with a control siRNA (siC samples) were used for comparison. Duplicate samples were analyzed. Transcriptomic analysis was performed by RNA-Seq
Publication Title
ERRα induces H3K9 demethylation by LSD1 to promote cell invasion.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina Genome Analyzer
Description
Glucocorticoid resistance (GCR) is defined as an unresponsiveness to the anti-inflammatory properties of glucocorticoids (GCs) and their receptor, the glucocorticoid receptor (GR). It is a serious problem in the management of inflammatory diseases and occurs frequently. The strong pro-inflammatory cytokine TNF induces an acute form of GCR, not only in mice, but also in several cell lines, e.g. in the hepatoma cell line BWTG3, as evidenced by impaired Dexamethasone (Dex)-induced GR-dependent gene expression. We report that TNF has a significant and broad impact on the transcriptional performance of GR, but no impact on nuclear translocation, dimerization or DNA binding capacity of GR. Proteome-wide proximity-mapping (BioID), however, revealed that the GR interactome is strongly modulated by TNF. One GR cofactor that interacts significantly less with the receptor under GCR conditions is p300. NF?B activation and p300 knockdown both reduce transcriptional output of GR, whereas p300 overexpression and NF?B inhibition revert TNF-induced GCR, which is in support of a cofactor reshuffle model. This hypothesis is supported by FRET studies. This mechanism of GCR opens new avenues for therapeutic interventions in GCR diseases Overall design: Examination of GR induced gene expression in 4 conditions (1 control: NI and 3 treated: DEX, TNF, TNFDEX) starting from 3 biological replicates
Publication Title
TNF-α inhibits glucocorticoid receptor-induced gene expression by reshaping the GR nuclear cofactor profile.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Arabidopsis thaliana
- 9 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
This experiment was set up in order to identify the (direct) transcriptional targets of the Ethylene Response Factor 115 (ERF115) transcription factor. Because ERF115 expression occurs in quiescent center (QC) cells and strong effects on the QC cells were observed in ERF115 overexpression plants, root tips were harvested for transcript profiling in order to focus on root meristem and QC specific transcriptional targets.
Publication Title
ERF115 controls root quiescent center cell division and stem cell replenishment.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Mesenchymal progenitor cells can be differentiated in vitro into myotubes that exhibit many characteristic features of primary mammalian skeletal muscle fibers. However, in general, they do not show the functional excitation-contraction coupling or the striated sarcomere arrangement typical of mature myofibers. Epigenetic modifications have been shown to play a key role in regulating the progressional changes in transcription necessary for muscle differentiation. In this study, we demonstrate that treatment of murine C2C12 mesenchymal progenitor cells with 10 M of the DNA methylation inhibitor 5-azacytidine (5AC) promotes myogenesis, resulting in myotubes with enhanced maturity as compared to untreated myotubes. Specifically, 5AC treatment resulted in the upregulation of muscle genes at the myoblast stage while at later stages nearly 50 % of the 5AC-treated myotubes displayed a mature, well-defined sarcomere organization as well as spontaneous contractions that coincided with action potentials and intracellular calcium transients. Both the percentage of striated myotubes and their contractile activity could be inhibited by 20 nM TTX, 10 M ryanodine and 100 M nifedipine, suggesting that action potential-induced calcium transients are responsible for these characteristics. Our data suggest that genomic demethylation induced by 5AC overcomes an epigenetic barrier that prevents untreated C2C12 myotubes from reaching full maturity.
Publication Title
Epigenetics: DNA demethylation promotes skeletal myotube maturation.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
- IlluminaHiSeq2000
Description
Genetic studies in T-cell acute lymphoblastic leukemia have uncovered a remarkable complexity of oncogenic and loss-of-function mutations. Amongst this plethora of genetic changes, NOTCH1 activating mutations stand out as the most frequently occurring genetic defect, identified in more than 50% of T-cell acute lymphoblastic leukemias, supporting an essential driver role for this gene in T-cell acute lymphoblastic leukemia oncogenesis. In this study, we aimed to establish a comprehensive compendium of the long non-coding RNA transcriptome under control of Notch signaling. For this purpose, we measured the transcriptional response of all protein coding genes and long non-coding RNAs upon pharmacological Notch inhibition in the human T-cell acute lymphoblastic leukemia cell line CUTLL1 using RNA-sequencing. Similar Notch dependent profiles were established for normal human CD34+ thymic T-cell progenitors exposed to Notch signaling activity in vivo. In addition, we generated long non-coding RNA expression profiles (array data) from GSI treated T-ALL cell lines, ex vivo isolated Notch active CD34+ and Notch inactive CD4+CD8+ thymocytes and from a primary cohort of 15 T-cell acute lymphoblastic leukemia patients with known NOTCH1 mutation status. Integration of these expression datasets with publically available Notch1 ChIP-sequencing data resulted in the identification of long non-coding RNAs directly regulated by Notch activity in normal and malignant T-cell context. Given the central role of Notch in T-cell acute lymphoblastic leukemia oncogenesis, these data pave the way towards development of novel therapeutic strategies that target hyperactive Notch1 signaling in human T-cell acute lymphoblastic leukemia. Overall design: CUTLL1 cell lines were treated with Compound E (GSI) or DMSO (solvent control). Cells were collected 12 h and 48 h after treatment. This was performed for 3 replicates. RNA-sequencing was performed on these samples.
Publication Title
The Notch driven long non-coding RNA repertoire in T-cell acute lymphoblastic leukemia.
Sample Metadata Fields
No sample metadata fields
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