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accession-icon GSE104656
Effect of Pre- and Postnatal Exposure to urban PM2.5 on the Transcriptome of the Developing and Early-Life Mouse Lung
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Over the last years, evidence has grown that exposure to air pollution, in addition to impairing lung function and health in individuals of all age, can be linked to negative effects in newborn when present during pregnancy. Data suggests that intrauterine exposure of fetuses (exposure of the mother to air pollution during pregnancy) in fact exerts a negative impact on lung development. However, the means by which exposure during pregnancy affects lung development, have not been studied in depth yet. In this study, we investigated alterations of the transcriptome of the developing lung in a mouse model of gestational and early-life postnatal exposure to urban PM2.5 (from Sao Paulo, Brazil).

Publication Title

Pre- and postnatal exposure of mice to concentrated urban PM<sub>2.5</sub> decreases the number of alveoli and leads to altered lung function at an early stage of life.

Sample Metadata Fields

Specimen part

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accession-icon SRP073509
Quantitative Analysis of cortical transcriptomes through Next Generation Sequencing from wild-type mice, wild-type mice treated with IL1b, IL-1R8-/- mice and IL-1R8-/- mice treated with IL1b antagonist Anakinra
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Quantitative Analysis of cortical transcriptomes through Next Generation Sequencing (RNA-Seq) from wild-type mice, wild-type mice treated with IL1b (200 ng/mouse, 14h), IL-1R8-/- mice and IL-1R8-/- mice treated with IL1b antagonist Anakinra (25 mg/kg per day for 3 consecutive days, i.p. administration). mRNA profiles of cortical tissue from adult wild-type mice, wild-type mice treated with IL1b (200 ng/kg, 14h), IL-1R8-/- mice (Garlanda et al., 2004), and IL-1R8-/- mice treated with Anakinra (25 mg/kg per day for 3 consecutive days, i.p. administration) were generated by next-generation sequencing (RNA-seq) using Illumina HiSeq 2500 apparatus in paired-end configuration (2x125bp). Each condition was assessed in triplicate (12 mRNA-seq libraries) and, to reduce biological variability, each mRNA library was generated from pooled total RNA isolated from cortical tissue of 3 individual mice. In total, 9 mice per condition were used. Libraries were stranded and multiplexed. To increase sequencing depth, libraries were sequenced in two different lanes. All the libraries were loaded in each of the two lanes. Quality control of the raw data was performed with FastQC (http://www.bioinformatics.babraham.ac.uk/projects/fastqc/). Libraries were trimmed for adapter removal using Trimmomatic (Bolger et al., 2014) and mapped to reference genome (Ensembl GRCm38) using TopHat2 (Kim et al., 2013) and Bowtie2 (Langmead et al., 2009). Library sizes of primary mapped reads were between 70 and 96 million reads. Samtools was used to manipulate BAM files (Li et al., 2009). For calling of differentially expressed genes (DEG), mapped reads were counted with HTSeq v0.6.1 (Anders et al., 2014) and count tables were analysed using DeSeq2 v1.10.1 R-package (Love et al., 2014) with a design of one factor with four levels (“wild-type”, “wild-type + IL1?”, “IL-1R8-/-”, “IL-1R8-/- + Anakinra"), and differences between groups were tested using contrasts for wild-type + IL1b versus wild-type; IL-1R8-/- versus wild-type; IL-1R8-/- + Kineret versus wild-type. For consideration of differentially regulated genes between conditions, we used adjusted p-value < 0.1 or adjusted p-value < 0.05 as indicated in the manuscript. Overall design: mRNA profiles in adult mouse cerebral cortex of wild type (WT), WT mice treated with IL1b (200 ng/kg, 14h), IL-1R8-/- mice, and IL-1R8-/- mice treated with IL1b antagonist Anakinra (25 mg/kg per day for 3 consecutive days, i.p. administration) were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500. Each sample was prepared by pooling cortical tissue from 3 idenpendent mice.

Publication Title

Lack of IL-1R8 in neurons causes hyperactivation of IL-1 receptor pathway and induces MECP2-dependent synaptic defects.

Sample Metadata Fields

Treatment, Subject

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accession-icon SRP147554
Single cell RNA-sequencing of human fetal kidneys
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

10X-based scRNA-seq data human fetal kidneys at 5 different ages Overall design: w9, w11, w13, w16 and w18 human fetal kidneys

Publication Title

Single-cell transcriptomics reveals gene expression dynamics of human fetal kidney development.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE51798
Transcriptional dissection of pancreatic tumors engrafted in mice
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Engraftment of primary pancreas ductal adenocarcinomas (PDAC) in mice to generate patient derived xenograft (PDX) models is a promising platform to for biological and therapeutic studies in this disease. However, these models are still incompletely characterized. Here, we measured the impact of the murine environment on the gene expression of the engrafted human tumoral cells. We have analyzed gene expression profiles from 35 new PDX models and compared them with previously published microarray data from PDAC and hepatocellular carcinoma (HCC). Our results showed that PDX models derived from PDAC, or HCC, were clearly different to the cell lines derived from the same cancer tissues. Indeed, PDAC- and HCC-derived cell lines are indistinguishable one from the other based in their gene expression profiles. In contrast, the transcriptomes of PDAC and HCC PDX models are clearly different and more similar to their original tumor than to PDX models from the other tumor type. Interestingly, the main differences between pancreatic PDX models and human PDAC is the expression of genes involved in pathways related with extracellular matrix interactions and cell cycle regulation likely reflecting the adaptations of the tumors to the new environment. Furthermore, most of these differences are detected in the first passages after the tumor engraftment, indicating early phases of the adaptation process. In conclusion, different from conventional cancer cell lines, PDX models of PDAC retain similar gene expression profiles of PDAC. Expression changes are mainly related to genes involved in stromal pathways likely reflecting the adaptation to new environments. We also provide evidence of the stability of gene expression patterns over subsequent passages.

Publication Title

Transcriptional dissection of pancreatic tumors engrafted in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE32697
Thrombospondin-1 type 1 repeats in a model of inflammatory bowel disease: genetic profile and therapeutic effects
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Thrombospondin 1 (TSP-1) is an anti-angiogenic matricellular protein with regulatory functions in inflammation and cancer. The type 1 repeats (TSR) domains of TSP-1 have been shown to interact with a wide range of proteins that result in the anti-angiogenic and anti-tumor properties of TSP-1. To evaluate potential therapeutic effects of TSRs in inflammatory bowel disease, we conducted clinical, histological and gene microarray analyses on a mouse model of induced colitis.

Publication Title

Thrombospondin-1 type 1 repeats in a model of inflammatory bowel disease: transcript profile and therapeutic effects.

Sample Metadata Fields

Specimen part

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accession-icon SRP167244
Transitions in cell potency during early mouse development are driven by Notch
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The Notch signalling pathway plays fundamental roles in diverse developmental processes in metazoans, where it is important in driving cell fate and directing differentiation of various cell types. However, we still have limited knowledge about the role of Notch in early preimplantation stages of mammalian development, or how it interacts with other signalling pathways active at these stages such as Hippo. By using genetic and pharmacological tools in vivo, together with image analysis of single embryos and pluripotent cell culture, we have found that Notch is active from the 4-cell stage. Transcriptomic analysis in single morula identified novel Notch targets, such as early naïve pluripotency markers or transcriptional repressors such as TLE4. Our results reveal a previously undescribed role for Notch in driving transitions during the gradual loss of potency that takes place in the early mouse embryo prior to the first lineage decisions. Overall design: Transcriptomic analysis comparing single Rbpj mutant and control mouse morulae. RNA was isolated from individual E2.5 embryos from two litters. 3 mutant and 3 control embryos were used for analysis.

Publication Title

Transitions in cell potency during early mouse development are driven by Notch.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE80008
Systemic disease signature of human cutaneous leishmaniasis
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

In addition to the recently published in situ transcriptomics of LCL skin lesions (Novais et al., Khouri et al.), we herein present the first systemic disease signature of localized cutaneous leishmaniasis (LCL), using Affymetrix microarrays (HuGene 1.0) followed by systems biology analysis of the PBMC transciptome of LCL patients (n=18), as compared to healthy controls (n=12).

Publication Title

Systems Approach Reveals Nuclear Factor Erythroid 2-Related Factor 2/Protein Kinase R Crosstalk in Human Cutaneous Leishmaniasis.

Sample Metadata Fields

Specimen part, Disease stage

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accession-icon GSE17731
Selective boosting of transcriptional and behavioral responses to drugs of abuse by histone deacetylase inhibition
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Histone acetylation and other modifications of the chromatin are important regulators of gene expression and, consequently, may contribute to drug-induced behaviors and neuroplasticity. Previous studies have shown that a reduction on histone deacetylase (HDAC) activity results on the enhancement of some psychostimulant-induced behaviors. In the present study, we extend those seminal findings by showing that the administration of the HDAC inhibitor sodium butyrate enhances morphine-induced locomotor sensitization and conditioned place preference. In contrast, this compound has no effects on the development of morphine tolerance and dependence. Similar effects were observed for cocaine and ethanol-induced behaviors. These behavioral changes were accompanied by a selective boosting of a component of the transcriptional program activated by chronic morphine administration that included circadian clock genes and other genes relevant in addictive behavior. Our results support an specific role for histone acetylation and the epigenetic modulation of transcription at a reduced number of biologically relevant loci on non-homeostatic, long lasting, drug-induced behavioral plasticity. To further investigate the molecular bases of sodium butyrate action on long-lasting behavioral responses to morphine, we screened for potential substrates of their interaction by performing a genome-wide comparison of the striatal transcriptome after chronic administration of morphine in the absence or presence of sodium butyrate.

Publication Title

Selective boosting of transcriptional and behavioral responses to drugs of abuse by histone deacetylase inhibition.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE44855
Genomic landscape of transcriptional and epigenetic dysregulation in a mouse model of early onset Huntington's disease
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genomic landscape of transcriptional and epigenetic dysregulation in early onset polyglutamine disease.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE44306
Gene expression profile of N171-HD82Q hippocampus and cerebellum.
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Transcriptional dysregulation is an important early feature of polyglutamine diseases. One of its proposed causes is defective neuronal histone acetylation, but important aspects of this hypothesis, such as the precise genomic topography of acetylation deficits

Publication Title

Genomic landscape of transcriptional and epigenetic dysregulation in early onset polyglutamine disease.

Sample Metadata Fields

Sex, Age, Specimen part

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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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Developed by the Childhood Cancer Data Lab

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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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