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accession-icon SRP100404
novel patient-derived cell lines
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

novel patient-derived cell lines from primary human liver cancer and malignant liver metastasis

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE79156
Blockade of the neogenin-RGMb-BMP signaling hub inhibits allergen-induced airway hyperreactivtiy
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Bronchial asthma is associated with type 2 immune responses induced by components of adaptive as well as innate immunity. Although innate cytokines such as IL-25 have been shown to play key roles in development of airway hyperreactivity (AHR), little is known of innate molecules that regulate IL-25-mediated airway inflammation. We found that blockade of repulsive guidance molecule b (RGMb) in an experimental murine model of asthma blocked the development of AHR, a cardinal feature of asthma, and that RGMb is expressed on F4/80+CD11b+CD11cneg macrophages (RGMb+ macrophages), which accumulated in the lungs of OVA-sensitized and challenged mice, but not in nave mice. Moreover, we found that a large fraction of the RGMb+ macrophages expressed the IL-25 receptor IL-17RB and produced IL-13. IL-25 was critical for the development of AHR in our model, since mice deficient in IL-17RB did not develop AHR. Finally, treatment with anti-RGMb mAb during the challenge phase of the protocol after allergen sensitization effectively prevented the development of AHR and airway inflammation, suggesting for the first time that RGMb+ cells, including RGMb+ macrophages, play critical roles in allergen-induced asthma.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP162003
Liver macrophages regulate metabolism through non-inflammatory factors
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

It is currently debated as to whether liver macrophage (LM) activation from an anti-inflammatory to pro-inflammatory phenotype contributes to obesity-induced metabolic diseases. Here we report that LMs do not undergo a pro-inflammatory phenotype switch in obesity-induced insulin resistance in mice and humans. Remarkably, immune response related genes remained also unchanged in fly immune cells (haemocytes) upon high fat feeding. However, unbiased transcriptomic analyses revealed that LMs produce non-inflammatory factors, such as insulin like growth factor binding protein 7 (Igfbp7), that directly regulate liver metabolism. Using a unique method to manipulate gene expression only in LMs in vivo, we discovered that IGFBP7 specifically produced by LMs binds the insulin receptor and induces lipogenesis and gluconeogenesis, two major pathways increased in metabolic diseases. This study shows that macrophages could contribute to insulin resistance independently of their inflammatory status and that targeting non-inflammatory factors produced by macrophages might represent a better strategy than anti-inflammatory drugs to tackle metabolic diseases.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part, Disease

View Samples
accession-icon SRP158689
Influence of miR-21-regulated pathways on T cell responses
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goal of this study was to examine how miR-21 upregulation influences T cell responses. miR-21 was antagonized by lentiviral overexpression of anti-sense miR-21 during activation of naive CD4 T cells from healthy adults. On day 5 after activation, libraries of miR-21 high and miR-21 low cells were prepared using the Ovation Human FFPE RNA-Seq Library Systems (NuGEN) and sequenced on an Illumina HiSeq 2500.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon SRP195476
Liver macrophages in obese mice
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA sequencing data from liver macrophages isolated from ob/ob mice.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

View Samples
accession-icon SRP136274
Quantitative Analysis mRNAs and proteins from satellite cells of muscle with NO66f/f or NO66-/-
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

the functions of nucleolar protein 66 in satellite cells

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line

View Samples
accession-icon E-MEXP-1269
Transcription profiling by array of three human multiple myeloma cell lines treated with 5-aza-2-deoxycytidine and/or trichostatin A
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

To identify epigenetically silenced genes in multiple myeloma (MM) cell lines and to determine the effects of 5-aza-2-deoxycytidine and trichostatin A on gene expression. We treated 3 multiple myeloma cell lines (MM1, NCI-H929, U266) with 5-aza-2-deoxycytidine and/or trichostatin A.

Publication Title

Genome-wide transcriptional response to 5-aza-2'-deoxycytidine and trichostatin a in multiple myeloma cells.

Sample Metadata Fields

Specimen part, Disease, Cell line

View Samples
accession-icon SRP051359
Homo sapiens Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

investigation of lncRNAs deregulated in oncogenic induced senescence.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon E-MEXP-1333
Brain gene expression profiles of Cln1 and Cln5 deficient mice unravels common molecular pathways underlying neuronal degeneration in NCL diseases
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The neuronal ceroid lipofuscinoses (NCL) are a group of childhood inherited neurodegenerative disorders characterized by blindness, early dementia and pronounced cortical atrophy. The similar pathological and clinical profiles of different forms of NCL suggest that common disease mechanisms may be involved. Here, we have performed quantitative gene expression profiling of cortex from targeted knock out mice produced for Cln1 and Cln5 to explore NCL-associated molecular pathways. Combined microarray datasets from both mouse models exposed a common affected pathway: genes regulating cytoskeletal dynamics and neuronal growth cone stabilization display similar aberrations. We analyzed locus specific gene expression and showed regional clustering of Cln1 and three major genes of this pathway, further supporting a close functional relationship between the corresponding gene products, Cap1, Ptprf and Ptp4a2. The evidence from the gene expression data was substantiated by immunohistochemical staining data of Cln1-/- and Cln5-/- cortical neurons. These primary neurons displayed abnormalities in beta-tubulin and actin as well as abnormal intracellular distribution of growth cone associated proteins GAP-43, synapsin and Rab3. Our data provide the first evidence for a common molecular pathogenesis behind neuronal degeneration in CLN1 and CLN5. Since CLN1 and CLN5 code for proteins with distinct functional roles these data may have implications for other forms of NCL.

Publication Title

Brain gene expression profiles of Cln1 and Cln5 deficient mice unravels common molecular pathways underlying neuronal degeneration in NCL diseases.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

View Samples
accession-icon GSE134204
Expression data from whole human skin samples
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Comparison of skin samples (neck skin, non photoexposed) from aged women with various perceived age

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

View Samples
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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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