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accession-icon SRP185583
Vasculature-associated fat macrophages readily adapt to inflammatory and metabolic challenges
  • organism-icon Mus musculus
  • sample-icon 152 Downloadable Samples
  • Technology Badge IconNextSeq 500, Illumina HiSeq 2500

Description

We show that the epididymal white adipose tissue harbors 4 subpopulations of macrophages (VAM1, VAM2, PreVAM and DPs), 2 subpopulations of Dendritic Cells (CD11B+CD103- and CD11B-CD103+) and monocytes. VAMs display a gene signature enriched in pathways related to anti-inflammatory/ detoxifying and repair processes. Our gene expression work shows no evidence of an M2 to a Classically Activated/M1 shift during diet-induced obesity (DIO). Gene expression of VAMs or DP macrophages cannot be defined as M1 or M1-like. Our data are more compatible with the category of “Metabolically-activated” macrophages (MMe) Overall design: Examination of RNA expression changes in different epididymal adipose tissue myeloid subpopulations in lean versus obese animals harboring metabolic syndrome

Publication Title

Vasculature-associated fat macrophages readily adapt to inflammatory and metabolic challenges.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE42896
Expression data from Arabidopsis seedlings upon LRIS using NAA (1-Naphthaleneacetic acid) or non-auxin-like lateral root inducer naxillin
  • organism-icon Arabidopsis thaliana
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

The acquisition of water and nutrients by plant roots is a fundamental aspect of agriculture and strongly depends on root architecture. Root branching and expansion of the root system is achieved through the development of lateral roots and is to a large extent controlled by the plant hormone auxin. However, the pleiotropic effects of auxin or auxin-like molecules on root systems complicate the study of lateral root development. Here we describe a small-molecule screen in Arabidopsis thaliana that identified naxillin as what is to our knowledge the first non-auxin-like molecule that promotes root branching. By using naxillin as a chemical tool, we identified a new function for root cap-specific conversion of the auxin precursor indole-3-butyric acid into the active auxin indole-3-acetic acid and uncovered the involvement of the root cap in root branching. Delivery of an auxin precursor in peripheral tissues such as the root cap might represent an important mechanism shaping root architecture. To further explore the specificity of naxillin for lateral root development, we compared the early effects of naxillin at the transcriptome level with NAA (1-Naphthaleneacetic acid) in roots of 3-day-old seedlings after 2-h and 6-h treatment.

Publication Title

A role for the root cap in root branching revealed by the non-auxin probe naxillin.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE53827
CCR2+ vs. CCR2- murine hematopoietic stem cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Comparative analysis of FACS-sorted CCR2- and CCR2+ HSC in the steady state. CCR2+ HSC have fourfold higher proliferative rates than CCR2- HSC, are are biased towards the myeloid lineage and dominate the migratory HSC population.

Publication Title

Myocardial Infarction Activates CCR2(+) Hematopoietic Stem and Progenitor Cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP061546
A mechanism for expansion of the regulatory T cell repertoire and its role in enforcing self-tolerance.
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Thymic Treg cells, mature non-Treg CD4+ single positive thymocytes, peripheral (spleen) resting and activated Treg cells were sorted from Foxp3-gfp reporter (wid type, WT) mice or Foxp3 enhancer CNS3 knockout (KO, carrying the same GFP reporter) mice. Total RNA was extracted and used for RNA sequencing to assess gene expression profiles. Overall design: Two 6-8 week old littermates of male Foxp3-gfp and Foxp3?CNS3-gfp mice were used to sort Treg cells and conventional CD4+ T cells. Lymphocyte preparation and electronic sorting were performed at the same time. RNA extraction, SMART amplification, library preparation were conducted in parallel.

Publication Title

A mechanism for expansion of regulatory T-cell repertoire and its role in self-tolerance.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP062866
Profiling status epilepticus-induced changes in hippocampal RNA expression using high-throughput RNA sequencing
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Status epilepticus (SE) is a life-threatening condition that can give rise to a number of neurological disorders, including learning deficits, depression, and epilepsy. Many of the effects of SE appear to be mediated by alterations in gene expression. To gain deeper insight into how SE affects the transcriptome, we employed the pilocarpine SE model in mice and Illumina-based high-throughput sequencing to characterize alterations in gene expression from the induction of SE, to the development of spontaneous seizure activity. While some genes were upregulated over the entire course of the pathological progression, each of the three sequenced time points (12-hour, 10-days and 6-weeks post-SE) had a largely unique transcriptional profile. Hence, genes that regulate synaptic physiology and transcription were most prominently altered at 12-hours post-SE; at 10-days post-SE, marked changes in metabolic and homeostatic gene expression were detected; at 6-weeks, substantial changes in the expression of cell excitability and morphogenesis genes were detected.  At the level of cell signaling, KEGG analysis revealed dynamic changes within the MAPK pathways, as well as in CREB-associated gene expression. Notably, the inducible expression of several noncoding transcripts was also detected. These findings offer potential new insights into the cellular events that shape SE-evoked pathology.  Overall design: cDNA from two animals was pooled into two independent biological replicates for each timepoint (ie. two sets of two animals per experimental group: control, 12 hours, 10 days, 6 weeks). Samples were sequenced using a Genome Analyzer II (GAII) at a concentration of 10pM in each lane. Base-calling was conducted with the standard Illumina Analysis Pipeline 1.0 (Firescrest-Bustard). Eight FASTQ sequence files (sequencing reads plus quality information) were generated and mapped to the mouse genome (UCSC mm9) using the Bowtie algorithm with default settings. A C++ program was used to count the number of uniquely mapped reads within exons of Ref-Seq genes (UCSC Genome Browser mm9 annotation).

Publication Title

Status epilepticus stimulates NDEL1 expression via the CREB/CRE pathway in the adult mouse brain.

Sample Metadata Fields

Cell line, Subject, Time

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accession-icon GSE98751
Hippocampal Gene Expression Profile of Mitogen Stress activated Kinase 1 (MSK1) null mice.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Analysis of alterations in the hippocampus transcriptome caused by deletion of Mitogen Stress activated Kinase 1 (MSK1).

Publication Title

Mitogen- and Stress-Activated Protein Kinase 1 Regulates Status Epilepticus-Evoked Cell Death in the Hippocampus.

Sample Metadata Fields

Specimen part

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accession-icon GSE952
Transcriptome analysis in rat
  • organism-icon Rattus norvegicus
  • sample-icon 122 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

Large scale transcriptome analysis of Wistar and Sprague Dawley rat tissues.

Publication Title

Applications of a rat multiple tissue gene expression data set.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE109365
Gene expression in developing fibrotic lesions in tracheas of chlorine-exposed mice
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Chlorine is a widely used industrial chemical that is also considered a chemical threat agent. Inhalation of chlorine gas can cause acute injury to the respiratory tract, including the death of airway epithelial cells. Failure to efficiently repair the epithelial damage is associated with long-term respiratory abnormalities, including airway fibrosis. We previously developed a model of airway injury in which mice exposed to chlorine gas exhibit epithelial damage and develop fibrosis in large airways.

Publication Title

Inhibition of chlorine-induced airway fibrosis by budesonide.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon SRP052620
Genome-wide effect of inhibition of glutamine transporter ASCT2 in PC-3 cells by BenSer or GPNA
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

To determine the global effects of ASCT2 inhibition, we used next generation sequencing to determine mRNA expression changes in PC-3 cells treated with BenSer or GPNA for 48 h. Overall design: Examination of two different ASCT2 inhibitors BenSer and GPNA in prostate cancer cell line PC-3.

Publication Title

Targeting ASCT2-mediated glutamine uptake blocks prostate cancer growth and tumour development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE66107
Everolimus protects podocytes via stabilizing TUBB2B and DCDC2 expression
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Glomerular podocytes are highly differentiated cells that are key components of the kidney filtration units. The podocyte cytoskeleton builds the basis for the dynamic podocyte cytoarchitecture and plays a central role for proper podocyte function. Recent studies implicate that immunosuppressive agents including the mTOR-inhibitor everolimus have a protective role directly on the stability of the podocyte cytoskeleton. To elucidate mechanisms underlying mTOR-inhibitor mediated cytoskeletal rearrangements, we carried out microarray gene expression studies to identify target genes and corresponding pathways in response to everolimus. We analyzed the effect of everolimus in a puromycin aminonucleoside experimental in vitro model of podocyte injury. Upon treatment with puromycin aminonucleoside, microarray analysis revealed gene clusters involving cytoskeletal-associated pathways, adhesion, migration and extracellular matrix composition to be affected. Everolimus is capable of protecting podocytes from injury, both on the transcriptome and protein level. Rescued genes included TUBB2B and DCDC2, both involved in microtubule structure formation in neuronal cells but not identified in podocytes so far. Confirming gene expression data, Western-blot analysis in cultured podocytes showed an increase of TUBB2B and DCDC2 protein after everolimus treatment, and immunohistochemistry in healthy control kidneys confirmed a podocyte-specific expression. Microtubule-inhibitor experiments led to a maldistribution of TUBB2B and DCDC2 as well as an aberrant reorganization of the actin cytoskeleton. Tubb2bbrdp/brdp mice showed a delay in glomerular podocyte and capillary development. Taken together, our study suggests that off-target, non-immune mediated effects of the mTOR-inhibitor everolimus on the podocyte cytoskeleton might involve regulation of microtubules, revealing a potential novel role of TUBB2B and DCDC2 in glomerular podocyte development

Publication Title

Everolimus Stabilizes Podocyte Microtubules via Enhancing TUBB2B and DCDC2 Expression.

Sample Metadata Fields

Specimen part, Treatment

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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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