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accession-icon GSE89997
Expression data from 2 cohorts of human pancreatic ductal adenocarcinoma (PDAC) tumors
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

In this dataset, we included expression data obtained from 30 resected human PDAC tumors, to examine what genes are differentially expressed in different cohorts that might lead to various outcomes

Publication Title

Identification of unique neoantigen qualities in long-term survivors of pancreatic cancer.

Sample Metadata Fields

Specimen part

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accession-icon SRP076550
Genome-wide analysis of gene expression in infarcted and non-infarcted left ventricle from NEIL3-deficient mice subjected to myocardial infarction
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Myocardial infarction (MI) triggers a reparative response involving fibroblast proliferation and differentiation driving extracellular matrix modulation necessary to form a stabilizing scar. Recently, it was shown that a genetic variant of the base excision repair enzyme endonuclease VIII-like 3 (NEIL3) was associated with increased risk of MI in humans. Here, we report elevated myocardial NEIL3 expression in heart failure patients and marked myocardial upregulation of Neil3 following MI in mice, especially in a fibroblast-enriched cell fraction. Neil3-/- mice showed increased mortality after MI compared to WT, caused by myocardial rupture. Neil3-/- hearts displayed enrichment of mutations in genes involved in mitogenesis of fibroblasts and transcriptome analysis revealed dysregulated fibrosis. Correspondingly, proliferation of vimentin+ and aSMA+ (myo)fibroblasts was increased in Neil3-/- hearts following MI. We propose that NEIL3 operates in genomic regions crucial for regulation of cardiac fibroblast proliferation and thereby controls extracellular matrix modulation after MI. Overall design: RNA from infarcted and non-infarcted LV of WT and Neil3-/- C57BL/6 mice obtained three days after induced myocardial infarction were subjected to RNA sequencing using Illumina Hiseq 2000

Publication Title

NEIL3-Dependent Regulation of Cardiac Fibroblast Proliferation Prevents Myocardial Rupture.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE68801
Human Alopecia Areata Skin Biopsy Samples
  • organism-icon Homo sapiens
  • sample-icon 116 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling of scalp skin biopsies from patients with alopecia areata or normal healthy controls

Publication Title

Molecular signatures define alopecia areata subtypes and transcriptional biomarkers.

Sample Metadata Fields

Sex, Age, Disease, Subject

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accession-icon GSE32614
Effects of Aging and Anatomic Location on Gene Expression in Human Retina
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Objective: To determine the effects of age and topographic location on gene expression in human neural retina.

Publication Title

Effects of aging and anatomic location on gene expression in human retina.

Sample Metadata Fields

Sex, Age

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accession-icon SRP158325
Reproducibility of molecular phenotypes after long-term differentiation to Human iPSC-Derived Neurons: a multi-site omics study [bulk]
  • organism-icon Homo sapiens
  • sample-icon 449 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Reproducibility in molecular and cellular studies is fundamental to scientific discovery. To establish the reproducibility of a well-defined long term neuronal differentiation protocol, we repeated the cellular and molecular comparison of the same two iPSC lines across five distinct laboratories. Despite uncovering acceptable variability within individual laboratories, we detect poor cross-site reproducibility of the differential gene expression signature between these two lines. Factor analysis identifies the laboratory as the largest source of variation along with several variation-inflating confounds such as passaging effects and progenitor storage. Single cell transcriptomics shows substantial cellular heterogeneity underlying inter-laboratory variability and being responsible for biases in differential gene expression inference. Factor analysis-based normalization of the combined dataset can remove the nuisance technical effects, enabling the execution of robust hypothesis generating studies. Our study shows that multi-center collaborations can expose systematic biases and identify critical factors to be standardized when publishing novel protocols, contributing to increased cross-site reproducibility. Overall design: RNAseq profiles of 57 bulk Human iPSC-Derived Neurons differentiated across five laboratories were generated in triplicates at two different time points and sequenced on 1 lane of HiSeq4000 at 75bp paired end. RNAseq profiles of .... single cells extracted from 2 of the 5 laboratories at the later time point were isolated by FACS onto 96-well plates and sequenced on 1 lane of HiSeq4000 at 75bp paired end.

Publication Title

Reproducibility of Molecular Phenotypes after Long-Term Differentiation to Human iPSC-Derived Neurons: A Multi-Site Omics Study.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE60499
Expression data from PKM1 or PKM2 expressing mouse embryonic fibroblasts.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We profiled global gene expression for two separate lines of mouse embryonic fibroblasts and find that deletion of PKM2 and expression of PKM1 does not alter global gene expression profiles.

Publication Title

Pyruvate kinase isoform expression alters nucleotide synthesis to impact cell proliferation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE14482
Differentially expressed genes in subpopulations of monocytes from non infected animals.
  • organism-icon Macaca mulatta
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rhesus Macaque Genome Array (rhesus)

Description

On the basis of the cell-surface molecule expression, CD16+ monocytes are likely comprised of distinct subpopulations of monocytes rather than a continuum of CD14+ monocytes with differing levels of cell activation. To better study this, we used gene array analysis that compared overall gene expression profiles of CD16+ subpopulations (CD14+CD16+ and CD16+) with that of CD14+CD16-. Gene expression in three FACS-sorted monocyte subsets was assessed by Affymetrix rhesus macaque oligonucleotide gene arrays that contain 52,024 probe sets covering 47,000 monkey genes. There were 29,361 probe sets that expressed in at least one subpopulation (raw array signal intensity > 32). Raw data were processed using robust multi-array average. To identify the most strongly, differentially expressed genes in each subpopulation, we only selected transcripts with consistently greater than four-fold difference (P < .05). In comparison to CD14+CD16- monocyte subset, a large number of genes (9098/29361, 30.9%) were differentially expressed in both CD14+CD16+ and CD16+ subsets: 1999 genes down-regulated; and 7099 genes up-regulated. Altogether, we observed large-scale gene expression differences between the CD14+CD16- subset and the two CD16+ subsets (CD14+CD16+ and CD16+), demonstrating transcriptional heterogeneity. The differential gene expression between CD16- and CD16+ monocytes underscore the fundamental differences between these cells.

Publication Title

Monocyte heterogeneity underlying phenotypic changes in monocytes according to SIV disease stage.

Sample Metadata Fields

Specimen part

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accession-icon SRP188078
NCBP2 modulates neurodevelopmental defects of the 3q29 deletion in Drosophila and Xenopus laevis models
  • organism-icon Drosophila melanogaster
  • sample-icon 66 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The 1.6 Mbp deletion on chromosome 3q29 is associated with a range of neurodevelopmental disorders, including schizophrenia, autism, microcephaly, and intellectual disability. Despite its importance towards neurodevelopment, the role of individual genes, genetic interactions, and disrupted biological mechanisms underlying the deletion have not been thoroughly characterized. Here, we used quantitative methods to assay Drosophila melanogaster and Xenopus laevis models with tissue-specific individual and pairwise knockdown of 14 homologs of genes within the 3q29 region. We identified developmental, cellular, and neuronal phenotypes for multiple homologs of 3q29 genes, potentially due to altered apoptosis and cell cycle mechanisms during development. Using the fly eye, we screened for 314 pairwise knockdowns of homologs of 3q29 genes and identified 44 interactions between pairs of homologs and 34 interactions with other neurodevelopmental genes. Interestingly, NCBP2 homologs in Drosophila (Cbp20) and X. laevis (ncbp2) enhanced the phenotypes of homologs of the other 3q29 genes, leading to significant increases in apoptosis that disrupted cellular organization and brain morphology. These cellular and neuronal defects were rescued with overexpression of the apoptosis inhibitors Diap1 and xiap in both models, suggesting that apoptosis is one of several potential biological mechanisms disrupted by the deletion. NCBP2 was also highly connected to other 3q29 genes in a human brain-specific interaction network, providing support for the relevance of our results towards the human deletion. Overall, our study suggests that NCBP2-mediated genetic interactions within the 3q29 region disrupt apoptosis and cell cycle mechanisms during development. Overall design: mRNA-sequencing of Drosophila neuron-specific RNAi knockdown (whole head) for four individual 3q29 homologs (DLG1, NCBP2, FBXO45, and PAK2), two pairwise knockdowns of 3q29 homologs (NCBP2/DLG1 and NCBP2/FBXO45), and two VDRC wild-type controls (GD and KK backgrounds). Sequencing was performed using Illumina HiSeq 2000 on three biological replicates per sample, with two-three technical replicates per biological replicate.

Publication Title

NCBP2 modulates neurodevelopmental defects of the 3q29 deletion in Drosophila and Xenopus laevis models.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE35896
Gene expression data from 62 colorectal cancers
  • organism-icon Homo sapiens
  • sample-icon 62 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We stratified colorectal tumor samples using a new unsupervised, iterative method based on non-negative matrix factorization (NMF). The resulting five subtypes exhibited activation of specific signaling pathways, and significant differences in microsatellite status and tumor location. We could also align three CRC cell lines panels to these subtypes.

Publication Title

Subtypes of primary colorectal tumors correlate with response to targeted treatment in colorectal cell lines.

Sample Metadata Fields

Sex, Race

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accession-icon GSE37320
Gene expression profiling of rhesus macaques vaccinated with ALVAC-SIVgpe DNA + SIVgp120 protein subunit and unvaccinated controls after challenge with SIVmac251
  • organism-icon Macaca mulatta
  • sample-icon 64 Downloadable Samples
  • Technology Badge Icon Affymetrix Rhesus Macaque Genome Array (rhesus)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Protection afforded by an HIV vaccine candidate in macaques depends on the dose of SIVmac251 at challenge exposure.

Sample Metadata Fields

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)

fund-icon Fund the CCDL

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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