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GSE73623
Sus scrofa
12 Downloadable Samples
Porcine Gene 1.0 ST Array (porgene10st)
Description
Expression data from valvular interstitial cells cultured in 2D or 3D PEG hydrogel systems compared to culture on tissue culture polystyrene and freshly isolated cells
Publication Title
Transcriptional profiles of valvular interstitial cells cultured on tissue culture polystyrene, on 2D hydrogels, or within 3D hydrogels.
Sample Metadata Fields
Specimen part
View Samples- Saccharomyces cerevisiae
- 4 Downloadable Samples
- Affymetrix Yeast Genome S98 Array (ygs98)
Description
The accumulation of unfolded proteins in the lumen of the endoplasmic reticulum (ER) causes stress and induces the unfolded protein response (UPR) which is characterised in part by the transcriptional induction of genes involved in assisting protein folding. Translational responses to ER stress have been less well described and here we report on a genome-wide analysis of translational regulation in the response to the ER stress-inducing agent dithiothreitol (DTT) in Saccharomyces cerevisiae. Although the observed polysome profiles were similar under control and ER stress conditions microarray analysis identified transcipt-specific translational regulation. Genes with functions in ribosomal biogenesis and assembly were translationally repressed under ER stress. In contrast mRNAs for known UPR genes, including the UPR transcription factor HAC1, the ER-oxidoreductase ERO1 and the ER-associated protein degradation (ERAD) gene DER1 were enriched in polysomal fractions under ER stress conditions. In addition, we show that splicing of HAC1 mRNA is required for efficient ribosomal loading and that Gcn2p is required for normal HAC1 splicing, so shedding light on the role of this protein kinase in the UPR pathway.
Publication Title
Transcript-specific translational regulation in the unfolded protein response of Saccharomyces cerevisiae.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Chromatin remodelling provides a key mechanism for the regulation of gene expression through dynamic alterations in nucleosome occupancy at promoters and enhancers. Haploinsufficiency for the ATP-dependent chromatin remodeller chromodomain-helicase-DNA-binding protein 7 (CHD7) causes human CHARGE syndrome. CHARGE is characterised by a distinct pattern of congenital anomalies, including cardiovascular malformations, and has traditionally been considered a neurocristopathy. We present a new perspective, by showing severe structural cardiovascular defects following ablation of Chd7 in the anterior mesoderm and other cardiac-related lineages. We identify multiple downstream pathways affected by the loss of Chd7 and disruption of excitation-contraction coupling in cardiomyocytes. Furthermore, we demonstrate CHD7 binding at the Sema3C promoter and alterations to the local chromatin structure in vivo, indicating direct transcriptional regulation. This work therefore provides novel insights into the etiology of heart defects arising in CHARGE syndrome and reveals a requirement for CHD7 activity in mesodermal cardiac progenitors.
Publication Title
A critical role for the chromatin remodeller CHD7 in anterior mesoderm during cardiovascular development.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
Description
Paternal imprinting initiates in primordial germ cells (PGCs), and is considered largely completed at birth. The resulting postnatal spermatogonial stem cells (SSCs) thenself-renew and proliferate to populate the testicular niche, with sexual maturation enabling productive gametogenesis. Overall design: mRNA profiles of neonatal wild type (WT) mice testis were generated by deep sequencing using Illumina HiSeq 2000 Examination of 2 different histone modifications in mouse spermatogonia Please note that ChIPSeq_Kitplus samples are samples isolated with MACS CD117 microbeads from Miltenyi and ChIPSeq_Kitminus are samples that were not positively selected for Kit.
Publication Title
Transcription and imprinting dynamics in developing postnatal male germline stem cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 4000
Description
Using our computational method SynGeNet to evaluate genomic and transcriptomic data characterizing four major genomic subtypes of melanoma, we selected the top ranked drug combination for BRAF-mutation melanoma for subsequent validaiton. Here we present drug-induced gene expression data from the BRAF-mutant A375 melanoma cell line in response to four treatment conditions: vehicle control (DMSO), vemurafenib alone, tretinoin (ATRA) alone and vemurafenib+tretinoin combination. Overall design: Gene expression profiles of A375 melanoma cells were generated by RNAseq (Illumina HiSeq 4000) under the following treatment conditions: vehicle control (DMSO), vemurafenib, tretinoin and vemurafenib + tretinoin combination.
Publication Title
Synergy from gene expression and network mining (SynGeNet) method predicts synergistic drug combinations for diverse melanoma genomic subtypes.
Sample Metadata Fields
Specimen part, Subject
View Samples- Danio rerio
- 5 Downloadable Samples
- Illumina HiSeq 2500
Description
The goal of this study was to investigate DNA methylation and gene expression changes in a zebrafish model of ICF Syndrome which were generated by mutation of ICF-gene zbtb24. Comparison of gene expression changes between wildtype and zbtb24 homozygous mutants revealed upregulation of interferon response genes following zbtb24 deletion. Upregulation of interferon response genes was blocked by mutation of the dsRNA helicase Mda5. Overall design: For RNA-seq, gene expression was compared in whole two-week-old zebrafish larvae that were wildtype or homozygous for the zbtb24mk22 mutant allele. We further performed RNA-Seq analysis in three-week-old zebrafish larvae that were WT, mda5mk29/mk29 , zbtb24mk22/mk22 and mda5mk29/mk29 ;zbtb24mk22/mk22. Three samples consisting of pools of 10 larvae were examined for each genotype. For ERRBS, DNA was separately isolated from the fins of three wildtype and three zbtb24mk22 homozygous mutant adults.
Publication Title
Pericentromeric hypomethylation elicits an interferon response in an animal model of ICF syndrome.
Sample Metadata Fields
Subject
View Samples- Ovis aries
- 8 Downloadable Samples
- Ovine Gene 1.1 ST Array (ovigene10st)
Description
study investigating the initiation of systemic inflammatory signaling in fetuses exposed to TLR-4 agonist lipopolysaccharides from E.coli
Publication Title
Outside-in? Acute fetal systemic inflammation in very preterm chronically catheterized sheep fetuses is not driven by cells in the fetal blood.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 31 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
The majority of NK cells (~90%) are phenotypically characterized as CD56dimCD16+, while the remaining are CD56brightCD16-. The cytotoxic CD56dimCD16+ NK subset expresses higher levels of chemokine receptors, and therefore is preferentially recruited to sites of inflammation. Encounters between CD56dimCD16+ NK cells with target cells and locally secreted inflammatory cytokines synergize to induce activation of this subset, leading to dramatically increased cytotoxic activity against target cells and abundant pro-inflammatory cytokine production often equivalent to that of the CD56brightCD16- population. The early recruitment of activation of CD56dimCD16+ NK cells to sites of inflammation raises many important questions regarding the potential immune functions of these cells that extend beyond their cytotoxic capabilities. This study has sought to elucidate the genetic profile of activated CD56dimCD16+ NK cells via a series of laboratory-based approaches coupled with a bioinformatics persective.
Publication Title
Gene expression profiling of the human natural killer cell response to Fc receptor activation: unique enhancement in the presence of interleukin-12.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
- IlluminaHiSeq2000
Description
Mitochondrial DNA (mtDNA) mutations cause inherited diseases and are implicated in the pathogenesis of common late-onset disorders, but it is not clear how they arise and propagate in the humans. Here we show that mtDNA mutations are present in primordial germ cells (PGCs) within healthy female human embryos. Close scrutiny revealed the signature of selection against non-synonymous variants in the protein-coding region, tRNA gene variants, and variants in specific regions of the non-coding D-loop. In isolated single PGCs we saw a profound reduction in the cellular mtDNA content, with discrete mitochondria containing ~5 mtDNA molecules during early germline development. Single cell deep mtDNA sequencing showed rare variants reaching higher heteroplasmy levels in later PGCs, consistent with the observed genetic bottleneck, and predicting >80% levels within isolated organelles. Genome-wide RNA-seq showed a progressive upregulation of genes involving mtDNA replication and transcription, linked to a transition from glycolytic to oxidative metabolism. The metabolic shift exposes deleterious mutations to selection at the organellar level during early germ cell development. In this way, the genetic bottleneck prevents the relentless accumulation of mtDNA mutations in the human population predicted by Muller's ratchet. Mutations escaping this mechanism will, however, show massive shifts in heteroplasmy levels within one human generation, explaining the extreme phenotypic variation seen in human pedigrees with inherited mtDNA disorders. Overall design: RNA-Seq and NGS analysis to investigate transcriptomes and mtDNA sequences of fetal hPGCs
Publication Title
Segregation of mitochondrial DNA heteroplasmy through a developmental genetic bottleneck in human embryos.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 274 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This experiment comprises 283 CEL files generated on the Affymetrix U133 Plus 2.0 gene expression microarray platform, using patient peripheral blood and bone marrow samples from the first cohort of patients accrued to Children's Oncology Group Study AALL0232. No clinical covariate data is provided at this time as the clinical study is not yet published. Researchers who would like to request outcome or other covariate data are asked to contact Dr. Cheryl Willman, cwillman@unm.edu, 505.272.5622 (University of New Mexico) and Dr. Steven Hunger, Stephen.Hunger@childrenscolorado.org (Children's Oncology Group and Children's Hospital Colorado) to arrange a collaboration.
Publication Title
Tyrosine kinome sequencing of pediatric acute lymphoblastic leukemia: a report from the Children's Oncology Group TARGET Project.
Sample Metadata Fields
Disease
View Samples