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accession-icon GSE18144
Array-based gene expression, CGH and tissue data define a 12q24 gain in neuroblastic tumors with prognostic implication
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Array-based gene expression, CGH and tissue data defines a 12q24 gain in neuroblastic tumors with prognostic implication.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment

View Samples
accession-icon GSE18139
Array-based gene expression in neuroblastic tumors
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Title: Array-based gene expression, CGH and tissue data define a 12q24 gain in neuroblastic tumors with prognostic implication.

Publication Title

Array-based gene expression, CGH and tissue data defines a 12q24 gain in neuroblastic tumors with prognostic implication.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE17987
Novel treatment of human pancreatic cancer using masitinib combined with standard gemcitabine chemotherapy
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Masitinib is a tyrosine kinase inhibitor of c-Kit, PDGFR and , and to some extent Lyn of the Src kinase family. We evaluated the therapeutic potential of masitinib in vitro on human pancreatic tumour cell lines and in vivo in a mouse model of human pancreatic cancer.

Publication Title

Masitinib combined with standard gemcitabine chemotherapy: in vitro and in vivo studies in human pancreatic tumour cell lines and ectopic mouse model.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE47440
The Y chromosome as a regulatory element shaping immune cell transcriptomes and susceptibility to autoimmune disease
  • organism-icon Mus musculus
  • sample-icon 36 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

The Y chromosome as a regulatory element shaping immune cell transcriptomes and susceptibility to autoimmune disease.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE47437
Lymph node CD4+ T cell and thioglycollate-elicited peritoneal macrophage expression data from nave young and old SJL/J and SJL-ChrY^B10.S male mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Understanding the DNA elements that constitute and control the regulatory genome is critical for the appropriate therapeutic management of complex diseases. Here, using chromosome Y (ChrY) consomic mouse strains on the C57BL/6J background, we show that susceptibility to two diverse animal models of autoimmune disease, including experimental allergic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in copy number of Sly and Rbmy multicopy ChrY genes. In the B6 background, ChrY possesses gene regulatory properties that impact both genome-wide gene expression and the presence of alternative splice variants in pathogenic CD4+ T cells. Using a ChrY consomic strain on the SJL background, we discovered a preference for ChrY-mediated gene regulation in macrophages, the immune cell subset underlying the EAE sexual dimorphism in SJL mice, rather than CD4+ T cells. Importantly, in both genetic backgrounds, an inverse correlation exists between the number of Sly and Rbmy ChrY gene copies and the number of significantly upregulated genes in immune cells, thereby supporting a link between copy number variation of Sly and Rbmy with the ChrY genetic element exerting regulatory properties. Moreover, in humans, an analysis of the CD4+ T cell transcriptome from male multiple sclerosis patients versus healthy controls provides further evidence for an evolutionarily conserved mechanism of gene regulation by ChrY. Thus, these data establish ChrY as a member of the regulatory genome in mammals due to its ability to regulate gene expression and alternative splicing in immune cells linked to disease.

Publication Title

The Y chromosome as a regulatory element shaping immune cell transcriptomes and susceptibility to autoimmune disease.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE47024
Lymph node CD4+ T cell expression data from nave C57BL/6J and C57BL/6J-ChrY^SJL
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Understanding the DNA elements that constitute and control the regulatory genome is critical for the appropriate therapeutic management of complex diseases. Here, using chromosome Y (ChrY) consomic mouse strains on the C57BL/6J background, we show that susceptibility to two diverse animal models of autoimmune disease, including experimental allergic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in copy number of Sly and Rbmy multicopy ChrY genes. In the B6 background, ChrY possesses gene regulatory properties that impact both genome-wide gene expression and the presence of alternative splice variants in pathogenic CD4+ T cells compared to CD4+ T cells. An inverse correlation exists between the number of Sly and Rbmy ChrY gene copies and the number of significantly upregulated genes in immune cells, thereby supporting a link between copy number variation of Sly and Rbmy and the ChrY genetic element exerting regulatory properties. Thus, these data establish ChrY as a member of the regulatory genome in mammals due to its ability to regulate gene expression and alternative splicing in immune cells linked to disease.

Publication Title

The Y chromosome as a regulatory element shaping immune cell transcriptomes and susceptibility to autoimmune disease.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE29681
Expression data from WT and R6/2 mice treated with HSP90 inhibitor NVP-HSP990
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Huntingtons disease (HD) is a neurodegenerative disorder that is associated with the deposition of proteinaceous aggregates in the brains of HD patients and mouse models. Previous studies have suggested that wide-scale disruption of protein homeostasis occurs in protein folding diseases. Protein homeostasis can be maintained by activation of the heat shock response (HSR) via the transcription factor heat shock factor 1 (HSF1), the pharmacological activation of which can be achieved by Hsp90 inhibition and has been demonstrated to be beneficial in cell and invertebrate models of HD. Whether the HSR is functional in HD and whether its activation has therapeutic potential in mammalian HD models is currently unknown. To address these issues, we used a novel, brain penetrant Hsp90 inhibitor to activate the HSR in brain after systemic administration. Microarrays, quantitative PCR and western blotting showed that the HSR becomes impaired with disease progression in two mouse models of HD and that this originates at the level of transcription.

Publication Title

Altered chromatin architecture underlies progressive impairment of the heat shock response in mouse models of Huntington disease.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

View Samples
accession-icon GSE69340
Expression data from cerebral cortices of bacTRAP transgenic mice
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We used microarrays of eight different cell types in cortex to conduct specificity index analysis for detailed cell type specific molecular profile.

Publication Title

Layer 2/3 pyramidal cells in the medial prefrontal cortex moderate stress induced depressive behaviors.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP056889
3'' RNA-seq of flies over-expressing cabut protein or RNAi against cabut mRNA
  • organism-icon Drosophila melanogaster
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

CbtOE (Tim-gal4; UAS-cbtFLAG), Tim-gal4 (control for CbtOE), cbtRNAi (Tim-gal4-UAS-Dcr2-UAS-cbtIR-cbtE1) and Tim-gal4;UAS-Dcr2 (control for CbtRNAi) flies. Flies were entrained in LD (light: dark) condition for 3-4 days and harvested at six time points: ZT3, ZT7, ZT11, ZT15, ZT19, ZT23 Fly heads were collected, RNA was extracted and RNA-seq libraries were prepared as previously described (Engreitz et al., 2013) Overall design: Three samples of cbtRNAi and three samples of their controls. Two samples of cbtOE with two samples of their controls.

Publication Title

The transcription factor Cabut coordinates energy metabolism and the circadian clock in response to sugar sensing.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon SRP043606
3'' RNA-seq of fly expressing cabut RNAi after exposure to different levels of sucrose
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Control (+/cbtE1-UAS-cbt RNAi) or cabut RNAi flies (Tim-gal4, UAS-cbt RNAi) were starved for 16 hours and then exposed to food containing different concentrations of sucrose: 0, 25, 50 and 100 % for 18 hours. Fly heads were collected, RNA was extracted and RNA-seq libraries were prepared as previously described (Engreitz et al., 2013) Overall design: For each sucrose concentration, two samples of cabut RNAi flies and one sample of control flies were sequenced.

Publication Title

The transcription factor Cabut coordinates energy metabolism and the circadian clock in response to sugar sensing.

Sample Metadata Fields

Specimen part, Subject

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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