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accession-icon GSE46287
A strong anti-inflammatory signature revealed by liver transcription profiling of Tmprss6-/- mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Tmprss6 is the master inhibitor of hepcidin and its inactivation causes iron refractory iron deficiency anemia both in human and in mice. Mice with iron deficiency anemia (IDA)-low hepcidin show a pro-inflammatory response that is blunted in iron deficienct-high hepcidin Tmprss6 null mice. We investigated the transcriptional response associated with chronic hepcidin overexpression by comparing whole genome transcription profiling of the liver of Tmprss6 KO mice and IDA animals, irrespective of iron deficiency.

Publication Title

A strong anti-inflammatory signature revealed by liver transcription profiling of Tmprss6-/- mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE972
NCSC-SC development
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Time course of early development of peripheral nerve, from embryonic day 9.5 to postnatal day 0.

Publication Title

Efficient isolation and gene expression profiling of small numbers of neural crest stem cells and developing Schwann cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP095117
Neural precursor cell-secreted TGF-ß2 subverts the inflammatory program of invading monocyte-derived dendritic cells during CNS autoimmunity
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

In Multiple Sclerosis, the pathological interaction of autoreactive helper T (TH) cells with mononuclear phagocytes in the central nervous system (CNS) drives initiation and maintenance of chronic neuroinflammation. Herein, we found that intrathecal transplantation of neural stem cells (NPCs) in mice with experimental autoimmune encephalomyelitis (EAE) impairs the accumulation of inflammatory monocyte-derived dendritic cells (moDCs) in the CNS leading to improved clinical outcome. NPCs treatment reduced in the CNS IL-23, IL-1 and TNF-a, cytokines required for terminal differentiation of TH cells and accordingly GM-CSF-producing pathogenic TH cells. In vivo and in vitro transcriptome analyses disclosed that NPC secreted factors induce an inhibition of DC differentiation and maturation, favoring a fate switch towards an anti-inflammatory phenotype. We identified TGF-ß2 as the crucial mediator of NPC immunomodulation: TGFß2 knockout NPCs transplanted in EAE are ineffective in impairing moDC accumulation within the CNS and fail to drive clinical improvement. This study provides evidence that intrathecally injected NPCs interfere with CNS-compartmentalized inflammation of the effector phase of EAE, reprogramming, through the secretion of TGF-ß2, inflammatory monocyte-derived DCs towards anti-inflammatory myeloid cells. Overall design: mRNA profiles of monocyte derived-dendritic cells (moDCs) isolated by FACS sorting at 7 days post-treatment from the CNS (hindbrain and spinal cord) of quadruplicate pool of 4–7 MOG35-55-immunized C57Bl/6 mice either intrathecally injected with PBS or 1 million neural precursor cells (NPCs) at the peak of the disease (2-4 days after clinical onset).

Publication Title

Neural precursor cell-secreted TGF-β2 redirects inflammatory monocyte-derived cells in CNS autoimmunity.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Cell line, Subject

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accession-icon GSE8514
Expression data from normal adrenal gland and aldosterone-producing adenoma
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The source of aldosterone in 30 to 40 % of patients with primary hyperaldosteronism (PA) is unilateral aldosterone-producing adenoma (APA). The mechanisms causing elevated aldosterone production in APA are unknown. Herein, we examined expression of G-protein coupled receptors (GPCR) in APA and demonstrate that compared to normal adrenals there is a general elevation of certain GPCR in many APA and/or ectopic expression of GPCR in others. RNA samples from normal adrenals (n = 5), APAs (n = 10), and cortisol-producing adenomas (CPAs) (n=13) were used on 15 genomic expression arrays, each of which included 223 GPCR transcripts presented in at least one out of 15 of the independent microarrays. The array results were confirmed using real-time RT-PCR (qPCR). Four GPCR transcripts exhibited a statistically significant increase that was greater than 3-fold compared to normal adrenals, suggesting a general increase in expression compared to normal adrenal glands. Four GPCR transcripts exhibited a greater than 15-fold increase of expression in one or more of the APA samples compared to normal adrenals. qPCR analysis confirmed array data and found the receptors with the highest fold increase in APA expression to be luteinizing hormone receptor (LH-R), serotonin receptor 4 (HTR4), gonadotropin-releasing hormone receptor (GnRHR), glutamate receptor metabotropic 3 (GRM3), endothelin receptor type B-like protein (GPR37), and ACTH receptor (MC2R). There are also sporadic increased expressions of these genes in the CPAs. Together, these findings suggest a potential role of altered GPCR expression in many cases of PA and provide candidate GPCR for further study.

Publication Title

G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP162582
Transcription factors activate genes through the phase separation capacity of their activation domains [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gene expression is controlled by transcription factors (TFs) that consist of DNA-binding domains (DBDs) and activation domains (ADs). The DBDs have been well- characterized, but little is known about the mechanisms by which ADs effect gene activation. Here we report that diverse ADs form phase-separated condensates with the Mediator coactivator. For the OCT4 and GCN4 TFs, we show that the ability to form phase-separated droplets with Mediator in vitro and the ability to activate genes in vivo are dependent on the same amino acid residues. For the estrogen receptor (ER), a ligand-dependent activator, we show that estrogen enhances phase separation with Mediator, again linking phase separation with gene activation. These results suggest that diverse TFs can interact with Mediator through the phase-separating capacity of their ADs and that formation of condensates with Mediator is involved in gene activation. Overall design: RNA-seq in mouse embryonic stem cells after OCT4 degradation or LIF withdrawal

Publication Title

Transcription Factors Activate Genes through the Phase-Separation Capacity of Their Activation Domains.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE48680
Glucocorticoid effect on mRNA translation in childhood acute lymphoblastic leukemia
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [CDF: huex10stv2_67_020 (huex10st)

Description

Glucocorticoids (GCs) are a central component in treating childhood acute lymphoblastic leukemia (chALL). They mainly act via regulating gene transcription. However, control of mRNA translation by GC has never been assessed systematically. In our research, T- and precursor B-ALL cells were cultured with and without GC for 6 hours and subjected to translational profiling, a technique combining sucrose gradient fractionation and microarray analysis of mRNA in different fractions. Analysis of GC regulation in different pools revealed no significant differences in regulation of mRNA translation by GC, suggesting no evidence for translational regulation by GC.

Publication Title

Translational profiling in childhood acute lymphoblastic leukemia: no evidence for glucocorticoid regulation of mRNA translation.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP137822
Coactivator condensation at super-enhancers links phase separation and gene control (RNA-Seq)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Super-enhancers (SEs) are clusters of enhancers that cooperatively assemble a high density of transcriptional apparatus to drive robust expression of genes with prominent roles in cell identity. We recently proposed that a phase-separated multi-molecular assembly underlies the formation and function of SEs. Here, we demonstrate that the SE-enriched factors BRD4 and MED1 form nuclear puncta that occur at SEs and exhibit properties of liquid-like condensates. Disruption of BRD4 and MED1 puncta by 1,6-hexanediol is accompanied by a loss of BRD4 and MED1 at SEs and a loss of RNAPII from SE-driven genes. We find that the intrinsically disordered regions (IDRs) of BRD4 and MED1 are sufficient to form phase-separated droplets in vitro and the MED1 IDR promotes phase separation in living cells. The MED1 IDR droplets are capable of compartmentalizing BRD4 and other transcriptional machinery in nuclear extracts. These results support the idea that SEs form phase-separated condensates that compartmentalize the transcription apparatus at key genes, provide insights into the role of cofactor IDRs in this process, and offer new insights into mechanisms involved in control of key cell identity genes. Overall design: polyA RNA-Seq in mouse embryonic stem cells

Publication Title

Coactivator condensation at super-enhancers links phase separation and gene control.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE109371
Glucose-dependent insulinotropic polypeptide ameliorates obesity and insulin resistance by attenuating S100A8/9 in myeloid cells
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Clariom S Array (clariomsmouse)

Description

Our data mark GIP as a beneficial immunoregulator during obesity and suggest a novel untapped therapeutic potential for specific targeted GIP analogs.

Publication Title

Glucose-Dependent Insulinotropic Polypeptide Receptor Deficiency Leads to Impaired Bone Marrow Hematopoiesis.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE73355
The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The goal of this study was to assess whether the presence of HLA-B*35 contributes to activation of ER stress/UPR and inflammation in lcSScPAH PBMC.

Publication Title

The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients.

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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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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