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accession-icon SRP135815
WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from the knockout of Hira in undifferentiated mouse embryonic stem cells (mESCs) and in day 15 differentiated cardiomyocytes.Methods: RNA extraction was done in duplicate from WT and Hira-null mESCs at day0 and day15 using TRIzol reagent. RNAseq was done onIllumina Nextseq500 and processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R2 package. Gene lists were filtered using adjusted p-value = 0.05 and absolute fold change = 2. Results:We identified 1680 transcripts changed in the absence of HIRA in day 15 differentiated cardiomyocytes. GO term cardiovascular system development was the most downregulated gene set(p-value = 0.01 and FDR =0.1. Conclusion: this study analysis the role of HIRA in early cardiac mesoderm development usinf an invitro mESCs model. Overall design: mRNA profile of WT(control) and Hira-null (KO) undifferentiated mESCs and mESCs- derived cardiomyocytes at day15 were generated by deep sequencing in duplicates using Illumina Nextseq 500 platform.

Publication Title

HIRA directly targets the enhancers of selected cardiac transcription factors during in vitro differentiation of mouse embryonic stem cells.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP072877
Mesp1Cre;Hira-/fl and Mesp1Cre;Hira+/fl in heart at E11.5 and E12.5
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from a Mesp1Cre driven ablation of Hira in the heart at E11.5 and E12.5. Methods: RNA extraction was done in triplicate from Mesp1Cre;Hira-/fl and Mesp1Cre;Hira+/fl embryonic hearts at E11.5 and E12.5 using the QIAGEN RNeasy mini kit. RNAseq was processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R package. Strand NGS 2.5 software was used to re-analyse the aligned files (.bam). By applying the Mann Whitney unpaired test, Benjamini Hochberg False discovery rate (FDR) and filtering the genes using adjusted p-value = 0.05 and absolute fold change = 1.5, 95 % of the results were identical to the DEseq package used by the UCL Genomics facility. Results: We identified 360 coding transcripts changed in the mutant hearts (Mann Whitney unpaired test, Benjamini Hochberg FDR, p = 0.05, FC = 1.5) with no trend towards up- or down-regulation of global transcription (48.8% down vs 51.2% up) at E12.5. Conclusions: This work analyses the role of HIRA in mouse cardiac development. It was found that Tnni2 is the most upregulated gene in the absence of Hira. qRT-PCR validation of 25 targets. Little (<5%) or no variation of fold change between RNAseq and qRT-PCR data were observed. Overall design: Cardiac mRNA profiles of 11-day and 12-day embryonic days Mesp1Cre control (Ctrl) and Mesp1Cre;Hira-/fl (mut) were generated by deep sequencing, in triplicate, using Illumina GAIIx.

Publication Title

HIRA Is Required for Heart Development and Directly Regulates Tnni2 and Tnnt3.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE2634
Comparison of human and non-human primate gene expression profiles
  • organism-icon Macaca mulatta, Chlorocebus aethiops, Homo sapiens, Macaca fascicularis
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling is an important tool in the development of medical countermeasures against chemical warfare agents (CWAs). Non-human primates (NHPs), specifically the rhesus macaque (Macaca mulatta), the cynomologus macaque (Macaca fascicularis) and the African green monkey (Chlorocebus aethiops), are vital models in the development of CWA prophylactics, therapeutics, and diagnostics. However, gene expression profiling of these NHPs is complicated by the fact their genomes are not completely sequenced, and that no commercially available oligonucleotide microarrays (genechips) exist. We, therefore, sought to determine whether gene expression profiling of NHPs could be performed using human genechips. Whole blood RNA was isolated from each species and used to generate genechip probes. Hybridization of the NHP samples to human genechips (Affymetrix Human U133 Plus 2.0) resulted in comparable numbers of transcripts detected compared with human samples. Statistical analysis revealed intraspecies reproducibility of genechip quality control metrics; interspecies comparison between NHPs and humans showed little significant difference in the quality and reproducibility of data generated using human genechips. Expression profiles of each species were compared using principal component analysis (PCA) and hierarchical clustering to determine the similarity of the expression profiles within and across the species. The cynomologus group showed the least intraspecies variability, while the human group showed the greatest intraspecies variability. Intraspecies comparison of the expression profiles identified probesets that were reproducibly detected within each species. Each NHP species was found to be dissimilar to humans; the cynomologus group was the most dissimilar. Interspecies comparison of the expression profiles revealed probesets that were reproducibly detected in all species examined. These results show that human genechips can be used for expression profiling of NHP samples and provide a foundation for the development of tools for comparing human and NHP gene expression profiles.

Publication Title

Comparison of non-human primate and human whole blood tissue gene expression profiles.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP104758
RNA-sequencing of adult C57/Bl6 lymph nodes
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Given the increased T cell mediated DTH response to Candida albicans in female compared to male mice, we asked whether female and male lymphnodes differed in their expression of genes relevant to cell recruitment. Overall design: Pooled Lymph Nodes of C57Bl/6 Wild-type Female N=6, Wild-type Male N=6, or C57Bl/6 Four Core Genotype XY Male N=3 mice were analyzed by RNAseq for differences in gene expression.

Publication Title

Sex Differences in Mouse Popliteal Lymph Nodes.

Sample Metadata Fields

Age, Cell line, Subject

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accession-icon GSE80447
Expression data from proliferating and senescent IMR90 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Total RNA was isolated from proliferating and senescent IMR90 cells to compare gene-expression to the changes in nucleolus-association in proliferating and senescent IMR90 cells.

Publication Title

Nucleolus association of chromosomal domains is largely maintained in cellular senescence despite massive nuclear reorganisation.

Sample Metadata Fields

Specimen part

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accession-icon GSE12196
Rat exposure to RDX (3mg/kg or 18mg/kg; 0, 4, 24, 48 hr)
  • organism-icon Rattus norvegicus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

RDX (Hexahydro-1,3,5-trinitro-1,3,5-triazine) is a synthetic, high-impact, relatively stable explosive that has been in use since WWII. Exposure to RDX can occur either occupationally or through ordnance that lays unexploded on training ranges. The toxicology of RDX is dominated by acute tonic-clonic seizures at high doses, which remit when exposure is removed and internal RDX levels decrease. Sub-chronic studies have revealed few other toxic effects. The objective of this study was to examine the effect of a single oral dose of RDX on global gene expression in the mammalian brain and liver, using a rodent model.

Publication Title

Global gene expression in rat brain and liver after oral exposure to the explosive hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX).

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP062278
Human macrophage-Leishmania infectome
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq1500

Description

The goal of this study is to simultaneously interrogate host and parasite gene expression programs in human macrophages infected with the intracellular parasites from the genus Leishmania. We conducted high-resolution sequencing of the transcriptomes of human macrophages infected with Leishmania spp. using an RNA-seq approach. An array of computational tools was applied to map reads to the Leishmania and human genomes and reconstruct full-length transcripts. mRNA abundance was determined for Leishmania and human genes at various time points post-infection, enabling us to identify co-expression patterns that correlate with the biology of the parasite and to obtain a preliminary analysis of the dynamic nature of parasite and host cell gene expression programs in the context of infection. This study provides a solid framework for future functional and genomic studies of leishmaniasis as well as intracellular pathogenesis in general.

Publication Title

Dual Transcriptome Profiling of Leishmania-Infected Human Macrophages Reveals Distinct Reprogramming Signatures.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE2565
Phosgene exposure in the mouse lung
  • organism-icon Mus musculus
  • sample-icon 96 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Carbonyl chloride (phosgene) is a toxic industrial compound (TIC) widely used in industry for the production of synthetic products, such as polyfoam rubber, plastics, and dyes. Exposure to phosgene results in a latent (1-24 hr), potentially life-threatening pulmonary edema and irreversible acute lung injury. A genomic approach was utilized to investigate the molecular mechanism of phosgene-induced lung injury. CD-1 male mice were exposed whole-body to either air or a concentration x time (c x t) amount of 32 mg/m3 (8 ppm) phosgene for 20 min (640 mg x min/m3). Lung tissue was collected from air- or phosgene-exposed mice at 0.5, 1, 4, 8, 12, 24, 48, and 72 hr post-exposure. RNA was extracted from the lung and used as starting material for the probing of oligonucleotide microarrays to determine changes in gene expression following phosgene exposure. The data were analyzed using principal component analysis (PCA) to determine the greatest sources of data variability. A three-way analysis of variance (ANOVA) based on exposure, time, and sample was performed to identify the genes most significantly changed as a result of phosgene exposure. These genes were rank ordered by p-values and categorized based on molecular function and biological process. Some of the most significant changes in gene expression reflect changes in glutathione synthesis and redox regulation of the cell, including upregulation of glutathione S-transferase alpha-2, glutathione peroxidase 2, and glutamate-cysteine ligase, catalytic subunit (also known as -glutamyl cysteine synthetase). This is in agreement with previous observations describing changes in redox enzyme activity after phosgene exposure. We are also investigating other pathways that are responsive to phosgene exposure to identify mechanisms of toxicity and potential therapeutic targets.

Publication Title

Genomic analysis of murine pulmonary tissue following carbonyl chloride inhalation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE16561
Gene expression analysis of peripheral whole blood RNA following ischemic stroke
  • organism-icon Homo sapiens
  • sample-icon 63 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

The purpose of this project was to elucidate gene expression in the peripheral whole blood of acute ischemic stroke patients to identify a panel of genes for the diagnosis of acute ischemic stroke. Peripheral blood samples were collected in Paxgene Blood RNA tubes from stroke patients who were >18 years of age with MRI diagnosed ischemic stroke and controls who were non-stroke neurologically healthy. The results suggest a panel of genes can be used to diagnose ischemic stroke, and provide information about the biological pathways involved in the response to acute ischemic stroke in humans.

Publication Title

Genomic biomarkers and cellular pathways of ischemic stroke by RNA gene expression profiling.

Sample Metadata Fields

Sex, Age, Race

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accession-icon GSE13428
Gene Expression Profiling of Rat Hippocampus Following Exposure to the Acetylcholinesterase Inhibitor Soman
  • organism-icon Rattus norvegicus
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Soman (O-Pinacolyl methylphosphonofluoridate) is a potent neurotoxicant. Acute exposure to soman causes profound inhibition of the critical enzyme acetylcholinesterase, resulting in excessive levels of the neurotransmitter acetylcholine. Excessive acetylcholine levels cause convulsions, seizures, and respiratory distress. The initial cholinergic crisis can be overcome by rapid anti-cholinergic therapeutic intervention, resulting in increased survival. However, conventional treatments do not protect the brain from seizure-related damage, and thus neurodegeneration of soman-sensitive areas of the brain is a potential post-exposure outcome. We performed gene expression profiling of rat hippocampus following soman exposure to gain greater insight into the molecular pathogenesis of soman-induced neurodegeneration.

Publication Title

Gene expression profiling of rat hippocampus following exposure to the acetylcholinesterase inhibitor soman.

Sample Metadata Fields

Sex

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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