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SRP100940
Mus musculus
3 Downloadable Samples
Illumina HiSeq 2000
Description
5-hydroxymethylcytosine (5hmC) occurs at maximal levels in postmitotic neurons where its accumulation is cell specific and correlated with gene expression. Here we demonstrate that the distribution of 5hmC in CG and non-CG dinucleotides is distinct, and that it reflects the binding specificity and genome occupancy of methylcytosine binding protein 2 (MeCP2). In expressed gene bodies, accumulation of 5hmCG acts in opposition to 5mCG resulting in “functional” demethylation and diminished MeCP2 binding, thus facilitating transcription. Non-CG hydroxymethylation occurs predominantly in CA dinucleotides (5hmCA) and it accumulates in regions flanking active enhancers. In these domains, oxidation of 5mCA to 5hmCA does not alter MeCP2 binding or expression of adjacent genes. We conclude that the role of 5-hydroxymethylcytosine in postmitotic neurons is to functionally demethylate expressed gene bodies while retaining the role of MeCP2 in chromatin organization. Overall design: Examination of genome wide cytosine methylation and hydroxymethylation per context in cerebellar granule cells and their function in MeCP2 binding. Nuclear RNA-Seq dataset.
Publication Title
5-hydroxymethylcytosine accumulation in postmitotic neurons results in functional demethylation of expressed genes.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Studies investigating the causes of autism spectrum disorder (ASD) point to genetic as well as epigenetic mechanisms of the disease. Identification of epigenetic processes that contribute to ASD development and progression is of major importance and may lead to the development of novel therapeutic strategies. Here we identify the bromodomain and extra-terminal domain containing transcriptional regulators (BETs) as epigenetic drivers of an ASD-like disorder in mice. We found that the pharmacological suppression of the BET proteins by a novel, highly selective and brain-permeable inhibitor, I-BET858, leads to selective suppression of neuronal gene expression followed by the development of an autism-like syndrome in mice. Many of the I-BET858 affected genes have been linked to ASD in humans thus suggesting the key role of the BET-controlled gene network in ASD. Our studies also suggest that environmental factors controlling BET proteins or their target genes may contribute to the epigenetic mechanism of ASD.
Publication Title
Autism-like syndrome is induced by pharmacological suppression of BET proteins in young mice.
Sample Metadata Fields
Specimen part
View Samples- Macaca mulatta
- 6 Downloadable Samples
- Affymetrix Rhesus Macaque Genome Array (rhesus)
Description
Rhesus macaques (RMs) inoculated with live-attenuated Rev-Independent Nef simian immunodeficiency virus (Rev-Ind NefSIV) as adults or neonates controlled viremia to undetectable levels and showed no signs of immunodeficiency over 6-8 years of follow-up. We tested the capacity of this live-attenuated virus to protect RMs against pathogenic, heterologous SIVsmE660 challenges
Publication Title
Live attenuated Rev-independent Nef¯SIV enhances acquisition of heterologous SIVsmE660 in acutely vaccinated rhesus macaques.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 35 Downloadable Samples
- NextSeq 500
Description
Ultra low input sequencing of FACS sorted primary murine microglia from CSF-1 or IL-34 deficient forebrain and cerebella, at P8 and 9 weeks Overall design: Csf1fl/fl vs NesCreCsf1fl/fl: 3-4 biological replicates per timepoint per group; Il34wt/wt vs Il34Lacz/Lacz: 2-3 biological replicates per timepoint per group. P8, 9weeks
Publication Title
CSF-1 controls cerebellar microglia and is required for motor function and social interaction.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Homo sapiens
- 63 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The aim of this study was to identify new biomarkers and to investigate pathways involved in the progression of human carotid atheroma.
Publication Title
Identification of two genes potentially associated in iron-heme homeostasis in human carotid plaque using microarray analysis.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
This experiment was conducted to identify target genes of the peroxisome proliferator-activated receptor beta (PPARb) in skeletal muscle of transgenic mice that overexpressed PPARb.
Publication Title
The nuclear receptor PPARβ/δ programs muscle glucose metabolism in cooperation with AMPK and MEF2.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 40 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Chronic myeloid leukemia is a disease originated at the level of hematopoietic stem cell, characterized by the abnormal overproduction and accumulation, both in blood and bone marrow, of myeloid cells. Treatment options include tyrosine kinase inhibitors that inhibit BCR-ABL activity, however some patients develop resistance to these drugs and has been asociated to the stem cells
Publication Title
Global gene expression profiles of hematopoietic stem and progenitor cells from patients with chronic myeloid leukemia: the effect of in vitro culture with or without imatinib.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
Low Klf4 expression reproducibly gives rise to a homogeneous population of partially reprogrammed iPSCs. Upregulation of Klf4 allows these cells to resume reprogramming, indicating that they are paused iPSCs that remain on the path towards pluripotency. Paused iPSCs with different Klf4 expression levels remain at distinct intermediate stages of reprogramming.
Publication Title
Manipulation of KLF4 expression generates iPSCs paused at successive stages of reprogramming.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- IlluminaHiSeq2500
Description
Mitochondrial biogenesis and metabolism recently emerged as critical modulators of stemness properties and differentiation programmes. The increase in mitochondrial biogenesis and metabolic shift toward increased oxidative phosphorylations (OXPHOS) appear as hallmarks of stem cell differentiation processes. While several mechanisms support the involvement of mitochondrial biogenesis and function in the regulation of stem cell differentiation, the mechanisms triggering mitochondrial biogenesis in the context of cell differentiation remain elusive. In this study, we performed transcriptomic and bioinformatic analyses in order to get deeper insights into the cross-regulation of mitochondrial biogenesis and hepatogenic differentiation of human bone marrow mesenchymal stem cells (BM-MSCs). We identified a transcriptional regulatory network involved in the co-regulation of stem cell differentiation and mitochondrial biogenesis. Overall design: Transcriptomics analyses performed at early time points of the hepatogenic differentiation of BM-MSC
Publication Title
MPV17 does not control cancer cell proliferation.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
COUP-TFII, a member of the nuclear receptor superfamily plays a critical role in angiogenesis and organogenesis during embryonic development. Our results indicate that COUP-TFII expression is profoundly upregulated in prostate cancer patients and might serves as biomarker for recurrence prediction. Thus we conduct transcriptome comparison of control and COUP-TFII depleted PC3 cells to gain genomic insights on the biological processes that COUP-TFII is involved in prostate cancer cells. Ingenuity Pathway Analysis (IPA) shows that the most prominent altered pathways in the COUP-TFII depleted cells are related to cell growth; cell cycle progression and DNA damage response. Indeed many growth related genes including E2F1, p21, CDC25A, Cyclin A and Cyclin B are changed in COUP-TFII knockdown cells, suggesting that COUP-TFII might be an important regulator for prostate cancer cell growth. Further functional assays from cells and mice genetic studies confirm the hypothesis that COUP-TFII serve as the major regulator to control prostrate cancer growth. Together, results provide insight into the role of COUP-TFII in prostate tumorigenesis.
Publication Title
COUP-TFII inhibits TGF-β-induced growth barrier to promote prostate tumorigenesis.
Sample Metadata Fields
Specimen part, Cell line
View Samples