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SRP072352
Homo sapiens
12 Downloadable Samples
Illumina HiSeq 2500
Description
To study the host transcriptome of human fibroblasts after infection with T. gondii (Type I-RH). Overall design: Three bioloigcal replicates of uninfected HFFs and three biological replicates of T. gondii (Type I-RH) infected HFFs were sequenced using directional RNA-seq.
Publication Title
SMITE: an R/Bioconductor package that identifies network modules by integrating genomic and epigenomic information.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 41 Downloadable Samples
- Illumina HiSeq 2500
Description
We compare the CD4+ T cell transcriptome between obese and normal-weight children with asthma to identify molecules/pathways differentially expressed in obese asthmatic CD4+ T cells Overall design: CD4+ T cell transcriptome generated using Directional RNA-Seq library preparatio; A=Normal-weight, B=obese
Publication Title
CDC42-related genes are upregulated in helper T cells from obese asthmatic children.
Sample Metadata Fields
Sex, Age, Specimen part, Disease stage, Race, Subject
View Samples- Homo sapiens
- 67 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We performed DNA methylation (HELP array) and gene expression profiling in 69 samples of diffuse large B cell lymphoma (DLBCL). First, by gene expression, two molecular subtypes of DLBCL termed as "germinal center B cell-like" (GCB) and "activated B cell-like" (ABC) DLBCL were assigned to the 69 DLBCL cases. Then, the supervised analysis using HELP data revealed strikingly different DNA promoter methylation patterns in the two molecular DLBCL subtypes. These data provide epigenetic evidence that the DLBCL subtypes are distinct diseases that utilize different oncogenic pathways.
Publication Title
DNA methylation signatures define molecular subtypes of diffuse large B-cell lymphoma.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 29 Downloadable Samples
- Illumina HiSeq 2500
Description
Background: Preeclampsia, traditionally characterized by high blood pressure and proteinuria, is a common pregnancy complication, which affects 2-8% of all pregnancies. Although children born to women with preeclampsia have a higher risk of hypertension in later life, the mechanism of this increased risk is unknown. DNA methylation is an epigenetic modification that has been studied as a mediator of cellular memory of adverse exposures in utero. Since each cell type in the body has a unique DNA profile, cell subtype composition is a major confounding factor in studies of tissues with heterogeneous cell types. The best way to avoid this confounding effect is by using purified cell types. However, the use purified cell types in large cohort translational studies is difficult. The amnion, the inner layer of the fetal membranes of placenta, is derived from the epiblast and consists of two cell types, which are easy to isolate from the delivered placenta. In this study, we demonstrate the value of using amnion samples for DNA methylation studies, revealing distinctive patterns between fetuses exposed to preeclampsia or hypertension and fetuses from normal pregnancies. Results: We performed a genome-wide DNA methylation analysis, HELP-tagging, on 62 amnion samples from placentas of uncomplicated, normal pregnancies, and those with complications of preeclampsia or hypertension. Using a regression model approach, we found 123, 85 and 99 loci with high confidence hypertension-associated, proteinuria-associated and hypertension and proteinuria-associated DNA methylation changes, respectively. We also found that these differentially methylated regions overlap loci previously reported as differentially methylated regions in preeclampsia. Conclusions: Our findings support prior observations that preeclampsia is associated with changes of DNA methylation near genes that have previously been found to be dysregulated in preeclampsia. We propose that amnionic membranes represent a valuable surrogate fetal tissue on which to perform epigenome-wide association studies of adverse intrauterine conditions. Overall design: Directional RNA profiles of amnion membranes were generated by deep sequencing using Illumina HiSeq2500. Twenty-nine human amnion specimens were used: 12 control and 17 preeclampsia exposed.
Publication Title
Amnion as a surrogate tissue reporter of the effects of maternal preeclampsia on the fetus.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
In this study we present the first genome-wide expression profiling of peripheral B cells by massive parallel RNA sequencing in patients with allergic asthma validating the discovery potential of this approach in allergy. Overall design: RNA-seq was used to asses expression differences in B CD19 Lymphocytes from house dust mite allergic patients and healthy controls.
Publication Title
Genome-wide expression profiling of B lymphocytes reveals IL4R increase in allergic asthma.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 1000
Description
Background: Global DNA methylation contributes to genomic integrity by supressing repeat associated transposition events. Several chromatin factors are required in addition to DNA methyltransferases to maintain DNA methylation at intergenic and satellite repeats. Embryos lacking Lsh, a member of the SNF2 superfamily of chromatin helicases, are hypomethylated. The interaction of Lsh with the de novo methyltransferase, Dnmt3b, facilitates the deposition of DNA methylation at stem cell genes. We wished to determine if a similar targeting mechanism operates to maintain DNA methylation at repetitive sequences. Results: We used HELP-seq to map genome wide DNA methylation patterns in Lsh-/- and Dnmt3b-/- somatic cells. DNA methylation is predominantly lost from specific genomic repeats in Lsh-/- cells: LTR-retrotransposons, LINE-1 repeats and mouse satellites. RNA-seq experiments demonstrate that specific IAP (Intracisternal A-type particle) LTRs and satellites, but not LINE-1 elements, are aberrantly transcribed inLsh-/- cells. LTR hypomethylation in Dnmt3b-/- cells is moderate and hypomethylated repetitive elements (IAP, LINE-1 and satellite) are silent. Chromatin immunoprecipitation (ChIP) indicates that repressed LINE-1 elements gain H3K4me3, but H3K9me3 levels are unaltered in Lsh-/- cells, indicating that DNA hypomethylation alone is not permissive for their transcriptional activation. Mis-expressed IAPs and satellites lose H3K9me3 and gain H3K4me3 in Lsh-/- cells. Conclusions: Our study emphasizes that regulation of repetitive elements by DNA methylation is selective and context dependent. We propose a model where Lsh is specifically required at a precise developmental window to target de novo methylation to repeat sequences, which is subsequently maintained by Dnmt1 in somatic cells to enforce repeat silencing thus contributing to genomic integrity. Overall design: Two pairs of RNA samples compared: WT and Lsh-/- RNA isolations from tail-tip fibroblasts; WT and Lsh-/- RNA isolations from E13.5 mouse embryos.
Publication Title
Lsh regulates LTR retrotransposon repression independently of Dnmt3b function.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 25 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Acute Myeloid Leukemia (AML) is a heterogeneous disease from the molecular and biological standpoints, and even patients with a specific gene expression profile may present clinical and molecular heterogeneity. We studied the epigenetic profiles of a cohort of patients that shared a common gene expression profile but differed in that only half of them harbored mutations of the CEBPA locus, while the rest presented with silencing of this gene and co-expression of certain T cell markers. DNA methylation studies revealed that these two groups of patients could be readily segregated in an unsupervised fashion based on their DNA methylation profiles alone. Furthermore, CEBPA silencing was associated with the presence of an aberrant DNA hypermethylation signature, which was not present in the CEBPA mutant group. This aberrant hypermethylation occurred more frequently at sites within CpG islands. CEBPA silenced leukemias also displayed marked hypermethylation when compared with normal CD34+ hematopoietic cells, while CEBPA mutant cases showed only mild changes in DNA methylation when compared to these normal progenitors. Biologically, CEBPA silenced leukemias presented with a decreased response to myeloid growth factors in vitro.
Publication Title
Genome-wide epigenetic analysis delineates a biologically distinct immature acute leukemia with myeloid/T-lymphoid features.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
The association of cytosine methylation and gene expression in the human kidneys is yet to be determined, here we have 25 pairs of the methylation and gene expression profile.
Publication Title
Cytosine methylation changes in enhancer regions of core pro-fibrotic genes characterize kidney fibrosis development.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina MouseRef-8 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Redistribution of H3K27me3 upon DNA hypomethylation results in de-repression of Polycomb target genes.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina MouseRef-8 v2.0 expression beadchip
Description
DNA methylation and the Polycomb Repression System are epigenetic mechanisms that play important roles in maintaining transcriptional repression. Recent evidence suggests that DNA methylation can attenuate the binding of Polycomb protein components to chromatin and thus plays a role in determining their genomic targeting. However, whether this role of DNA methylation is important in the context of transcriptional regulation is unclear. By genome-wide mapping of the Polycomb Repressive Complex 2 (PRC2)-signature histone mark, H3K27me3, in severely DNA hypomethylated mouse somatic cells, we show that hypomethylation leads to widespread H3K27me3 redistribution, in a manner that reflects the local DNA methylation status in wild-type cells. Unexpectedly, we observe striking loss of H3K27me3 and PRC2 from Polycomb-target gene promoters in DNA hypomethylated cells, including Hox gene clusters. Importantly, we show that many of these genes become ectopically expressed in DNA hypomethylated cells, consistent with loss of Polycomb-mediated repression. An intact DNA methylome is required for appropriate Polycomb-mediated gene repression by constraining PRC2 targeting. These observations identify a previously unappreciated role for DNA methylation in gene regulation and therefore influence our understanding of how this epigenetic mechanism contributes to normal development and disease.
Publication Title
Redistribution of H3K27me3 upon DNA hypomethylation results in de-repression of Polycomb target genes.
Sample Metadata Fields
Specimen part
View Samples