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accession-icon SRP016518
The expression analyses of metafemales compared with normal females
  • organism-icon Drosophila melanogaster
  • sample-icon 43 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

Comapare the global expression of metafemales and normal femalems Overall design: Collected the metafemales, females and males and made RNA-seq

Publication Title

Dosage compensation and inverse effects in triple X metafemales of Drosophila.

Sample Metadata Fields

Sex, Subject

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accession-icon SRP021491
The expression analyses of trisomy 2L compared with normal
  • organism-icon Drosophila melanogaster
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

Dosage compensation was referred as an equalized X chromosome gene expression between males and females in Drosophila. And inverse dosage effects, produced by genomic imbalance, are believed to account for this modulated expression. Here we made a global expression comparison of trisomy 2L with on extra copy of chromosome 2 long arm to normal diploid with two copies of 2L with high throughput RNA-sequencing. We want to test how about the gene expression pattern changes in those comparisons, including the genes on varied chromosome 2 long arm, some other autosomal genes except chromosome 2L and X chromosome genes. Dosage compensation with an expression level similar to normal diploid and inverse dosage effects should be detected. Overall design: Comapare the global expression of trisomy 2L samples with the normal diploids Collected the females and males from trisomy 2L and Cantons and performed RNA-seq

Publication Title

Differential effect of aneuploidy on the X chromosome and genes with sex-biased expression in Drosophila.

Sample Metadata Fields

Sex, Subject

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accession-icon GSE41571
Genome-wide expression profiling of laser micro-dissected macrophages from ruptured and stable atherosclerotic human plaques
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Objective: Resident macrophages play an important role in atheromatous plaque rupture. The macrophage gene expression signature associated with plaque rupture is incompletely defined due to the complex cellular heterogeneity in the plaque. We aimed to characterise differential gene expression in resident plaque macrophages from ruptured and stable human atheromatous lesions. A cell-specific approach has the potential to address the question of gene expression differences between particular cell types in stable and unstable plaques with greater precision than approaches based on the study of whole plaques. Using laser micro-dissection, we isolated total RNA from macrophage-rich regions of stable and ruptured human atheromatous plaques derived from carotid endarterectomy samples which were comprehensively characterized using clinical, radiological and histological criteria, and carried out genome-wide gene expression profiling using microarrays.

Publication Title

Increased expression of fatty acid binding protein 4 and leptin in resident macrophages characterises atherosclerotic plaque rupture.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE50518
Shp2 Signaling Suppresses Senescence in PyMT-induced Mammary Gland Cancer in Mice
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Shp2 signaling suppresses senescence in PyMT-induced mammary gland cancer in mice.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE50517
Shp2 Signaling Suppresses Senescence in PyMT-induced Mammary Gland Cancer in Mice [Mouse430_2 array]
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In this study, we have used techniques from cell biology, biochemistry, and genetics to investigate the role of the tyrosine phosphatase Shp2 in tumor cells of MMTV-PyMT mouse mammary glands. Genetic ablation or pharmacological inhibition of Shp2 induces senescence, as determined by the activation of senescence-associated -gal (SA--gal), cyclin-dependent kinase inhibitor 1B (p27), p53, and histone 3 trimethylated lysine 9 (H3K9me3). Senescence induction leads to inhibition of self-renewal of tumor cells and blockage of tumor formation and growth. A signaling cascade was identified that acts downstream of Shp2 to counter senescence: Src, Focal adhesion kinase and Map kinase inhibit senescence by activating the expression of S-phase kinase-associated protein 2 (Skp2), Aurora kinase A (Aurka), and the Notch ligand Delta-like 1 (Dll1), which block p27 and p53. Remarkably, the expression of Shp2 and of selected target genes predicts human breast cancer outcome. We conclude that therapies which rely on senescence induction by inhibiting Shp2 or controlling its target gene products may be useful in blocking breast cancer.

Publication Title

Shp2 signaling suppresses senescence in PyMT-induced mammary gland cancer in mice.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE50516
Shp2 Signaling Suppresses Senescence in PyMT-induced Mammary Gland Cancer in Mice [Mouse430A_2 array]
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In this study, we have used techniques from cell biology, biochemistry, and genetics to investigate the role of the tyrosine phosphatase Shp2 in tumor cells of MMTV-PyMT mouse mammary glands. Genetic ablation or pharmacological inhibition of Shp2 induces senescence, as determined by the activation of senescence-associated -gal (SA--gal), cyclin-dependent kinase inhibitor 1B (p27), p53, and histone 3 trimethylated lysine 9 (H3K9me3). Senescence induction leads to inhibition of self-renewal of tumor cells and blockage of tumor formation and growth. A signaling cascade was identified that acts downstream of Shp2 to counter senescence: Src, Focal adhesion kinase and Map kinase inhibit senescence by activating the expression of S-phase kinase-associated protein 2 (Skp2), Aurora kinase A (Aurka), and the Notch ligand Delta-like 1 (Dll1), which block p27 and p53. Remarkably, the expression of Shp2 and of selected target genes predicts human breast cancer outcome. We conclude that therapies which rely on senescence induction by inhibiting Shp2 or controlling its target gene products may be useful in blocking breast cancer.

Publication Title

Shp2 signaling suppresses senescence in PyMT-induced mammary gland cancer in mice.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE107384
Genome-wide analysis of P8 sciatic nerve gene expression of control, Maf mutant and ErbB2 mutant mice
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Analysis of genes regulated by Maf and donwstream of ErbB2 in P8 Schwann cells

Publication Title

Maf links Neuregulin1 signaling to cholesterol synthesis in myelinating Schwann cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE54044
Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic -cell function (Expression data from islets of control and Insm1 conditional deleted adult pancreatic islets)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The zinc finger factor Insm1 is known to regulate differentiation of pancreatic cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic cells in mice.

Publication Title

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE35899
Expression data from Mammospheres
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The combined activation of Wnt/-catenin and MET/HGF is required for mammary cancer stem cell (MaCSC) maintenance. We generated mammospheres derived from tumors of mice harboring Wnt/Met signaling mutations on which we performed microarray analysis to evaluate gene expression signatures controlled by Wnt and MET pathways. We used the gene expression profiles to dissect the role and the functions of these pathways in MaCSCs.

Publication Title

Combined Wnt/β-catenin, Met, and CXCL12/CXCR4 signals characterize basal breast cancer and predict disease outcome.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP173598
A C/EBPa–Wnt connection in gut homeostasis and carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We explored the connection between C/EBPa (CCAAT/enhancer binding protein a) and Wnt signaling in gut homeostasis and carcinogenesis. C/EBPa was expressed in human and murine intestinal epithelia in the transit amplifying region of the crypts and was absent in intestinal stem cells and Paneth cells with activated Wnt signaling. In human colorectal cancer and murine APCMin/+ polyps, C/EBPa was absent from nuclear ß-catenin–positive tumor cells. In chemically induced intestinal carcinogenesis, C/EBPa KO in murine gut epithelia increased tumor volume. C/EBPa deletion extended the S-phase cell zone in intestinal organoids and activated typical proliferation gene expression signatures, including that of Wnt target genes. Genetic activation of ß-catenin in organoids attenuated C/EBPa expression. Comparing gene expression of wild type and C/EBPa KO organoids by RNA sequencing aimed to identify C/EBPa dependent alterations in gene expression. Overall design: These data suggest homeostatic and oncogenic suppressor functions of C/EBPa in the gut by restricting Wnt signaling.

Publication Title

A C/EBPα-Wnt connection in gut homeostasis and carcinogenesis.

Sample Metadata Fields

Specimen part, 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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