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E-MEXP-557
Arabidopsis thaliana
16 Downloadable Samples
Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Seven-day-old white-light-grown wild-type, cop1-4 or hy5-1 mutant Arabidopsis seedlings were exposed for fifteen minutes to polychromatic radiation with decreasing short-wave cut-off in the UV range (WG305 = +UV-B, WG327 = -UV-B) and samples were taken 1 h after the onset of irradiation.
Publication Title
CONSTITUTIVELY PHOTOMORPHOGENIC1 is required for the UV-B response in Arabidopsis.
Sample Metadata Fields
Age, Time
View Samples- Arabidopsis thaliana
- 20 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Seven-day-old white-light-grown Arabidopsis seedlings were exposed for 15 minutes to polychromatic radiation with decreasing short-wave cut-off in the UV range, transferred back to the standard growth chamber and samples were taken 1 and 6 hours after the start of irradiation.
Publication Title
Genome-wide analysis of gene expression reveals function of the bZIP transcription factor HY5 in the UV-B response of Arabidopsis.
Sample Metadata Fields
Age, Time
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Affymetrix Drosophila Genome Array (drosgenome1)
Description
The study of the role of Drosophila Ada2b SAGA histone acetyltransferase component at early pupal stage (P4)
Publication Title
Genes of the ecdysone biosynthesis pathway are regulated by the dATAC histone acetyltransferase complex in Drosophila.
Sample Metadata Fields
Sex, Age, Time
View Samples- Homo sapiens
- 4 Downloadable Samples
Affymetrix Human Gene 2.0 ST Array (hugene20st), Illumina HumanMethylation450 BeadChip (HumanMethylation450_15017482)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
No associated publication
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina HumanMethylation450 BeadChip (HumanMethylation450_15017482), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
We employed the AML cell line model U937 to determine the effects of single and dual treatment with the HMA decitabine and the HDACi Pano or VPA on gene expression and DNA methylation. We noted global alterations of gene expression and a massive effect on the methylome.
Publication Title
No associated publication
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
One major mode of action of DNA hypomethylating agents such as decitabine (DAC) is reactivation of gene expression and induction of differentiation. Prompted by observations of differentiation induction in leukemic myeloid cells and upregulation of fetal hemoglobin (HbF) in adult patients suffering from hemoglobinopathies, we aimed at systematically investigating the potential and significance of DAC for in vitro and in vivo induction of erythroid differentiation and HbF expression. In K562 (bcr-abl positive) and HEL (bcr-abl negative) myeloid leukemia cell line models, both with bilineage differentiation potential, erythroid differentiation and hemoglobin synthesis but not megakaryocytic differentiation could be induced by DAC treatment. The induction of erythroid differentiation was accompanied by a specific transcriptome signature that shared common patterns and groups of genes with the changes observed in K562 cells treated with the hemin, a known inducer of erythropoesis. Top regulated groups of transcripts in DAC treated cells were related to erythropoesis and iron metabolism. DAC treatment led to reactivation and upregulation of alpha globin and genes of the beta globin locus including the gamma globins resulting in HbF tetramer protein synthesis in K562 cells. This DAC-induced erythroid differentiation and HbF induction was accompanied by 2-3 fold upregulation of the key erythroid transcription factor GATA1. In contrast, PMA, an inducer of megakaryocytic differentiation, conversely led to a loss of GATA1 expression in K562 cells. Serial HbF measurements in DAC treated AML (n=25) and high-risk MDS (n=15) patients revealed that induction of HbF or persistent elevated HbF levels during treatment can also be detected in a significant proportion of patients in vivo (61,5%, p=0.033). Here, early HbF induction (after 2 courses) was significantly associated with platelet increment (rs=0.534, p=0.027) and strongly predicted neutrophil recovery (rs=0.554, p=0.021). The presence of elevated HbF levels in patients achieving CR upon DAC and exhibiting complete (cytogenetic) clearance of the malignant clone suggests that HbF induction does not occur in cells of the malignant clone but rather in non-malignant, polyclonal erythroid precursor cells. One major mode of action of DNA hypomethylating agents such as decitabine (DAC) is reactivation of gene expression and induction of differentiation. Prompted by observations of differentiation induction in leukemic myeloid cells and upregulation of fetal hemoglobin (HbF) in adult patients suffering from hemoglobinopathies, we aimed at systematically investigating the potential and significance of DAC for in vitro and in vivo induction of erythroid differentiation and HbF expression.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
The mechanisms involved in the pathogenesis of HD that result in late, and fatal, neurodegeneration are still not fully understood. The monogenic nature of HD is in contradiction with the complexity of the cellular alterations found in patients with HD. Huntingtin interacts with a broad range of proteins within the cell, and it is altered by the expanded polyglutamine tract. Transcriptional dysregulation is a common finding in genetic models and in human HD patients, and it is thought to play an important role in the disease. Although the onset of the disease is late in life, growing lines of evidence suggest that mHtt causes alterations in development. In this microarray study, the effects of mHtt on the transcriptome were investigated with a full-length human huntingtin (96 CAG repeats) expressing transgenic rat model of HD at an early stage of development (E14).
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
Illumina HiSeq 2000, Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Histone Deacetylases 1 and 2 Regulate Microglia Function during Development, Homeostasis, and Neurodegeneration in a Context-Dependent Manner.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples- Mus musculus
- 81 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
Recent studies have shown that tissue macrophages (MF) arise from embryonic progenitors of the yolk sac (YS) and fetal liver and colonize the tissues before birth. Further studies have proposed that developmentally distinct tissue MF can be identified based on the differential expression of F4/80 and CD11b, but whether a characteristic transcriptional profile exists is largely unknown. Here, we established an inducible fate mapping system that facilitated the identification of A2 progenitors of the YS as source of F4/80hi but not CD11bhi MF. Large-scale transcriptional profiling of MF precursors from the YS until adulthood allowed the description of a complex MF pedigree. We further identified a distinct molecular signature of F4/80hi and CD11bhi MF and found that Irf8 was vital for MF maturation and the innate immune response. Our data provide new cellular and molecular insights into the origin and developmental pathways of tissue MF.
Publication Title
Transcriptome-based profiling of yolk sac-derived macrophages reveals a role for Irf8 in macrophage maturation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Microglia are tissue macrophages of the central nervous system (CNS) that control tissue homeostasis, and as such they are crucially important for organ integrity. Microglia dysregulation is thought to be causal for a group of neuropsychiatric, neurodegenerative and neuroinflammatory diseases, called microgliopathies. However, how the intracellular stimulation machinery in microglia is controlled is poorly understood. By using expression studies, we identified the ubiquitin-specific protease (Usp) 18 in white matter microglia that essentially contributes to microglial quiescence under homeostatic conditions. We further found that microglial Usp18 negatively regulated the activation of STAT1 and concomitant induction of interferon-induced genes thereby disabling the termination of IFN signalling. Unexpectedly, the Usp18-mediated feedback loop was independent from the catalytic domain of the protease but instead required the interacting region of Ifnar2. Additionally, the absence of Ifnar1 completely rescued microglial activation indicating a tonic IFN signal mediated by receptor interactions under non-diseased conditions. Finally, conditional depletion of Usp18 only in myeloid cells significantly enhanced the disease burden in a mouse model of CNS autoimmunity, increased axonal and myelin damage and determined the spatial distributions of CNS lesions that shared the same STAT1 signature as myeloid cells found in active multiple sclerosis (MS) lesions. These results identify Usp18 as novel negative regulator of microglia activation, demonstrate a protective role of the IFNAR pathway for microglia and establish Usp18 as potential therapeutic target for the treatment of MS.
Publication Title
USP18 lack in microglia causes destructive interferonopathy of the mouse brain.
Sample Metadata Fields
Specimen part
View Samples