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accession-icon GSE31113
Molecular Organization of Drosophila Neuroendocrine Cells by DIMMED: Global Profiling of Pan-Neuronal DIMMED Expression Effects
  • organism-icon Drosophila melanogaster
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

To amass candidate DIMM targets in addition to Phm (Park et al., 2008a), we used genome-wide microarray profiling by over-expressing DIMM throughout the embryonic nervous system. We compared profiles from experimental (elav>dimm) and control (elav-GAL4) embryos at 22-26 hr and 28-32 hr after egg laying (AEL). The design was intended to identify transcripts consistently up-regulated shortly after the induction of DIMM; in so doing, we could circumvent the lethality that ensues in late embryonic, and/ or by early larval stages, due to pan-neuronal DIMM expression.

Publication Title

Molecular organization of Drosophila neuroendocrine cells by Dimmed.

Sample Metadata Fields

Specimen part

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accession-icon GSE55028
CMPF alters expression of genes related to metabolism in isolated mouse islets
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

CMPF is elevated in diabetes and is associated with impaired insulin secretion. We used microarrays to determine the effect of CMPF on gene expression in isolated islets.

Publication Title

The furan fatty acid metabolite CMPF is elevated in diabetes and induces β cell dysfunction.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE66099
Unique Patients from the Genomics of Pediatric SIRS and Septic Shock Investigators (GPSSSI)
  • organism-icon Homo sapiens
  • sample-icon 272 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This dataset is composed of the unique patients (276; at the Day 1 timepoint) that are present in the six other GEO datasets published by Hector Wong and the Genomics of Pediatric SIRS and Septic Shock Investigators. This dataset thus includes all unique patients from GSE4607, GSE8121, GSE9692, GSE13904, GSE26378, and GSE26440. These are only from the Day 1 timepoint.

Publication Title

A comprehensive time-course-based multicohort analysis of sepsis and sterile inflammation reveals a robust diagnostic gene set.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE69815
Expression array of glucosamine-fed Drosophila heart/nephrocyte complexes
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Examined the expression effects of supplementing Drosophila food on heart and nephrocyte complexes

Publication Title

Diet-Induced Podocyte Dysfunction in Drosophila and Mammals.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE53509
Drosophila CNS mitochondrial DNA dysfunction microarray
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Drosophila Gene 1.0 ST Array (drogene10st)

Description

Mitochondrial DNA (mtDNA) encodes essential components of the respiratory chain and loss of mtDNA leads to mitochondrial dysfunction and neurodegeneration. Mitochondrial transcription factor A (TFAM) is an essential component of mtDNA replication and a regulator of mitochondrial copy number in cells. Studies have shown that TFAM knockdown leads to mitochondrial dysfunction and respiratory chain deficiencies. ATP synthase is Complex V of the mitochondrial respiratory chain. It is driven by a proton gradient between the intermembrane space and the mitochondrial matrix and generates the majority of cellular ATP. The knockdown of coupling factor 6 (Cf6), one of the components of the proton channel F0, causes dysfunction in the complex, leading to mitochondrial dysfunction and respiratory chain deficiencies. Using gene expression analysis, we aimed to investigate the effects of mtDNA dysfunction in the CNS at the molecular level.

Publication Title

Mitochondrial retrograde signaling regulates neuronal function.

Sample Metadata Fields

Specimen part

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accession-icon SRP023262
A shared transcriptional program in early breast neoplasias despite genetic and clinical distinctions
  • organism-icon Homo sapiens
  • sample-icon 80 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

The earliest recognizable stages of breast neoplasia are lesions that represent a heterogeneous collection of epithelial proliferations currently classified based on morphology. Their role in the development of breast cancer is not well understood but insight into the critical events at this early stage will improve efforts in breast cancer detection and prevention. These microscopic lesions are technically difficult to study so very little is known about their molecular alterations. To characterize the transcriptional changes of early breast neoplasia, we sequenced 3''- end enriched RNAseq libraries from formalin-fixed paraffin-embedded tissue of early neoplasia samples and matched normal breast and carcinoma samples from 25 patients. We find that gene expression patterns within early neoplasias are distinct from both normal and breast cancer patterns and identify a pattern of pro-oncogenic changes, including elevated transcription of ERBB2, FOXA1, and GATA3 at this early stage. We validate these findings on a second independent gene expression profile data set generated by whole transcriptome sequencing. Measurements of protein expression by immunohistochemistry on an independent set of early neoplasias confirms that ER pathway regulators FOXA1 and GATA3, as well as ER itself, are consistently upregulated at this early stage. The early neoplasia samples also demonstrate coordinated changes in long non-coding RNA expression and microenvironment stromal gene expression patterns. This study is the first examination of global gene expression in early breast neoplasia, and the genes identified here represent candidate participants in the earliest molecular events in the development of breast cancer. Overall design: 3SEQ was performed on 72 FFPE human breast samples from 25 patients: 24 normal, 25 early neoplasia, 9 carcinoma in situ, and 14 invasive cancer

Publication Title

A shared transcriptional program in early breast neoplasias despite genetic and clinical distinctions.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

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accession-icon GSE70271
caArray_jacks-00113: Murine KRASLA lung cancer gene expression
  • organism-icon Mus musculus
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Tumors from 5-6 month old KrasLA mice were dissected. Gene expression analysis on U74A affy chips. 19 normal lungs from age matched controls were also includeed

Publication Title

Comparison of gene expression and DNA copy number changes in a murine model of lung cancer.

Sample Metadata Fields

Sex, Age, Disease, Disease stage

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accession-icon GSE17049
Parasite strain-specific pathogenesis in murine infections with Trypanosoma brucei
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Different strains of T. brucei induce different degrees of pathology in infected animals, and TREU927-infected mice display greater splenomegaly and anaemia than 247-infected mice. The analysis of differential host gene expression in infected spleens has allowed the identification of which pathways or processes are crucial in determining the progression of disease, for example IL10, LXR/RXR activation and alternative macrophage activation.

Publication Title

Role for parasite genetic diversity in differential host responses to Trypanosoma brucei infection.

Sample Metadata Fields

Specimen part

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accession-icon SRP043043
Global analysis of ZNF217 chromatin occupancy in the breast cancer cell genome reveals an association with Eralpha
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Background: The ZNF217 gene, encoding a C2H2 zinc finger protein, is located at 20q13 and found amplified and overexpressed in greater than 20% of breast tumors. Current studies indicate ZNF217 drives tumorigenesis, yet the regulatory mechanisms of ZNF217 are largely unknown. Because ZNF217 associates with chromatin modifying enzymes, we postulate that ZNF217 functions to regulate specific gene signaling networks. Here, we present a large-scale functional genomic analysis of ZNF217, which provides insights into the regulatory role of ZNF217 in MCF7 breast cancer cells. Results: ChIP-seq analysis reveals that the majority of ZNF217 binding sites are located at distal regulatory regions associated with the chromatin marks H3K27ac and H3K4me1. Analysis of ChIPseq transcription factor binding sites shows clustering of ZNF217 with FOXA1, GATA3 and ERalpha binding sites, supported by the enrichment of corresponding motifs for the ERalpha-associated cisregulatory sequences. ERalpha expression highly correlates with ZNF217 in lysates from breast tumors (n=15), and ERalpha co-precipitates ZNF217 and its binding partner CtBP2 from nuclear extracts. Transcriptome profiling following ZNF217 depletion identifies differentially expressed genes co-bound by ZNF217 and ERalpha; gene ontology suggests a role for ZNF217-ERalpha in expression programs associated with ER+ breast cancer studies found in the Molecular Signature Database. Data-mining of expression data from breast cancer patients correlates ZNF217 with reduced overall survival in multiple subtypes. Conclusions: Our genome-wide ZNF217 data suggests a functional role for ZNF217 at ERalpha target genes. Future studies will investigate whether ZNF217 expression contributes to aberrant ERalpha regulatory events in ER+ breast cancer and hormone resistance Overall design: Differential RNA-seq profiling from triplicate biological replicates of MCF7 cells treated with scrambled siRNA or siZNF217.

Publication Title

Global analysis of ZNF217 chromatin occupancy in the breast cancer cell genome reveals an association with ERalpha.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE42678
Human epidermal neural crest stem cells (hEPI-NCSC) - expanded versus pre-differentiated into neural stem cell-like cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

hEPI-NCSC are neural crest derived multipotent somatic stem cells that persist in hair follicle stem cell niche, termed the bulge, and persist into adulthood (Clewes O et al, 2011). The purpose of this project was to generate two gene expression profiles, (1) of ex vivo expanded hEPI-NCSC (XP) and (2) of cells, whihc after expansion were grown in a culture medium (NP1), which was empirically designed to pre-differentiate the multipotent stem cells into neural stemcell like cells.

Publication Title

Differentiation of human epidermal neural crest stem cells (hEPI-NCSC) into virtually homogenous populations of dopaminergic neurons.

Sample Metadata Fields

Sex, Specimen part

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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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