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accession-icon GSE23206
NSCLC cells treated with Gefitinib
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

About 10% of all NSCLC patients respond to gefitnib treatment and all of these patients will acquire resistance to the EGFR TKI.

Publication Title

Rapidly acquired resistance to EGFR tyrosine kinase inhibitors in NSCLC cell lines through de-repression of FGFR2 and FGFR3 expression.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE54015
Expression data from male and female Schlager hypertensive (BPH/2J) and normotensive (BPN/3J) kidneys
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Analysis of kidneys from 12 week BPH/2J hypertensive and age matched normotensive BPN/3J controls - males and females. The results provide insights into the genes that are involved in hypertension in both males and females, as well as highlight mechanisms that underlye sex differences in hypertension.

Publication Title

Identification of genes with altered expression in male and female Schlager hypertensive mice.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE57613
Hypoxia regulates alternative splicing of HIF and non-HIF target genes
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Human Exon 1.0 ST Array (huex10st)

Description

Alternative RNA splicing analysis in Hep3B cell cultured under 21% (N1,3,5) or 1.2% (H2,4,6) oxygen

Publication Title

Hypoxia regulates alternative splicing of HIF and non-HIF target genes.

Sample Metadata Fields

Cell line

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accession-icon SRP029933
Technical Variations in Low-Input RNA-seq Methodologies
  • organism-icon Mus musculus
  • sample-icon 52 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcriptomics data obtained from limiting amounts of mRNA is often noisy, providing primarily qualitative changes in transcript expressions. So far, technical variations arising out of the library preparation protocols have not been adequately characterized at reduced levels of mRNA. Here, we generated sequencing libraries from limiting amounts of mRNA using three amplification-based methods, viz. Smart-seq, DP-seq and CEL-seq, and demonstrated significant technical variations in these libraries. Reduction in mRNA levels led to inefficient amplification of the majority of low to moderately expressed transcripts. Furthermore, stochasticity in primer hybridization and/or enzyme incorporation was magnified during the amplification step resulting in significant distortions in fold changes of the transcripts. Consequently, the majority of the differentially expressed transcripts identified were either high-expressed and/or exhibited high fold changes. High technical variations, which were sequencing depth independent, ultimately masked subtle biological differences mandating the development of improved amplification-based strategies for quantitative transcriptomics from limiting amounts of mRNA. Overall design: Sequencing libraries were prepared from serial dilutions of mRNA, ranging from 1 ng to 25 pg, using three amplification-based methods, viz. Smart-seq, DP-seq and CEL-seq. The mRNA was derived from an in vitro model of lineage segregation achieved by modulating TGF beta signaling pathway in differentiating mouse embryonic stem cells.

Publication Title

Technical variations in low-input RNA-seq methodologies.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE25076
Hypothalamic expression differences between hypertensive BPH/2J and normotensive BPN/3J mouse strains
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Identification of hypothalamic genes whose expression differs between high blood pressure (BPH/2J) and normal blood pressure (BPN/3J) Schlager mouse strains at age 6 weeks (young) and 26 weeks (mature) using Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

Publication Title

Global identification of the genes and pathways differentially expressed in hypothalamus in early and established neurogenic hypertension.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE26007
Hypothalamic expression differences between hypertensive BPH/2J during circadian variations of blood pressure
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Identification of hypothalamic genes whose expression differs between active (peak of blood pressure) and inactive periods in the high blood pressure (BPH/2J) Schlager mouse, adjusted by their age- and activity-matched normal blood pressure (BPN/3J) controls using Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

Publication Title

Genes influencing circadian differences in blood pressure in hypertensive mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE81248
Gene expression data from HEY cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The innate immune system is vital to rapidly responding to pathogens and Toll-like receptors (TLRs) are a critical component of this response. Nanovesicular exosomes play a role in immunity, but to date their exact contribution to the dissemination of the TLR response is unknown. To understand the effect of exosomal cargo released from locally stimulated cells on distal cell expression, we collected exosomes from local ovarian adenocarcinoma (HEY) cells that were either unstimulated (control-exosomes), stimulated with pIC (pIC-exosomes), or lipopolysaccharide (LPS-exosomes) for 48 hours. The three groups of exosomes were added to nave (distal) cells and the gene expression profiles were compared between local TLR stimulation (for 6 hours) and distal stimulation mediated by exosomes at the 48-hour time point

Publication Title

TLR-exosomes exhibit distinct kinetics and effector function.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE21138
Gene Expression Profiles in BA46 of Subjects with Schizophrenia and Matched Controls
  • organism-icon Homo sapiens
  • sample-icon 57 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Results from clinical and imaging studies provide evidence for changes in schizophrenia with disease progression, however, the underlying molecular differences that may occur at different stages of illness have not been investigated. To test the hypothesis that the molecular basis for schizophrenia changes from early to chronic illness, we profiled genome-wide expression patterns in prefrontal cortex of schizophrenic subjects at different stages of illness, along with their age- and sex-matched controls. Results show that gene expression profiles change dramatically depending on the stage of illness, whereby the greatest number and magnitude of gene expression differences were detected in subjects with short-term illness ( 4 years from diagnosis). Comprehensive pathways analyses revealed that each defined stage of illness was associated with dysfunction in both distinct, as well as overlapping systems. Short-term illness was particularly associated with disruptions in gene transcription, metal ion binding, RNA processing and vesicle-mediated transport. In contrast, long-term illness was associated with inflammation, stimulus-response and immune functions. We validated expression differences of 12 transcripts associated with these various functions by real-time PCR analysis. While only four genes, SAMSN1, CDC42BPB, DSC2 and PTPRE, were consistently expressed across all groups, there was dysfunction in overlapping systems among all stages, including cellular signal transduction, lipid metabolism and protein localization. Our results demonstrate that the molecular basis for schizophrenia changes from early to chronic stages, providing evidence for a changing nature of schizophrenia with disease progression.

Publication Title

Molecular profiles of schizophrenia in the CNS at different stages of illness.

Sample Metadata Fields

Sex, Age

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accession-icon GSE62923
The Activation-Induced Assembly of an RNA/Protein Interactome Centered on the Splicing Factor U2AF2 Regulates Gene Expression in Human CD4 T Cells
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The Activation-Induced Assembly of an RNA/Protein Interactome Centered on the Splicing Factor U2AF2 Regulates Gene Expression in Human CD4 T Cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE62921
The Activation-Induced Assembly of an RNA/Protein Interactome Centered on the Splicing Factor U2AF2 Regulates Gene Expression in Human CD4 T Cells [total RNA-array]
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Illumina HiSeq 2000

Description

Activation of CD4 T cells is a reaction to challenges such as microbial pathogens, cancer and toxins that defines adaptive immune responses. The roles of T cell receptor crosslinking, intracellular signaling, and transcription factor activation are well described, but the importance of post-transcriptional regulation by RNA-binding proteins (RBPs) has not been considered in depth. We describe a new model expanding and activating primary human CD4 T cells and applied this to characterizing activation-induced assembly of splicing factors centered on U2AF2. We immunoprecipitated U2AF2 to identify what mRNA transcripts were bound as a function of activation by TCR crosslinking and costimulation. In parallel, mass spectrometry revealed the proteins incorporated into the U2AF2-centered RNA/protein interactome. Molecules that retained interaction with the U2AF2 complex after RNAse treatment were designated as central interactome members (CIMs). Mass spectrometry also identified a second class of activation-induced proteins, peripheral interactome members (PIMs), that bound to the same transcripts but were not in physical association with U2AF2 or its partners. siRNA knockdown of two CIMs and two PIMs caused changes in activation marker expression, cytokine secretion, and gene expression that were unique to each protein and mapped to pathways associated with key aspects of T cell activation. While knocking down the PIM, SYNCRIP, impacts a limited but immunologically important set of U2AF2-bound transcripts, knockdown of U2AF1 significantly impairs assembly of the majority of protein and mRNA components in the activation-induced interactome. These results demonstrated that CIMs and PIMs, either directly or indirectly through RNA, assembled into activation-induced U2AF2 complexes and play roles in post-transcriptional regulation of genes related to cytokine secretion. These data suggest an additional layer of regulation mediated by the activation-induced assembly of RNA splicing interactomes that is important for understanding T cell activation.

Publication Title

The Activation-Induced Assembly of an RNA/Protein Interactome Centered on the Splicing Factor U2AF2 Regulates Gene Expression in Human CD4 T Cells.

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)

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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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