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accession-icon GSE57547
6KR-EGFR expressing MCF7 following EGF or HRG stimulation
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

EGF and HRG, growth factor ligands for EGFR and ErbB3/4 receptor, induce transient and sustained ERK activity associated with cellular proliferation and differentiation of MCF-7 cells, respectively. To rigorously analyze the effect of ERK signal duration for mRNA expression dynamics and its relationship with cell determination, we modified the EGF-triggered ERK signal duration by changing the EGFR activation dynamics by impairing the ubiquitination and degradation process. Mutation of the six lysine residues (6KR; K692, K713, K730, K843, K905 and K946) of the EGFR responsible for ubiquitin conjugation has shown sustained phosphorylation of the receptor (Huang et al, 2006; Goh et al, 2010). Therefore we constructed the MCF-7 cell lines that stably express 6KR EGFR (6KR), and analyzed signaling and mRNA expression dynamics in response to EGF and HRG.

Publication Title

Feedforward regulation of mRNA stability by prolonged extracellular signal-regulated kinase activity.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Cell line, Race, Time

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accession-icon GSE13009
MCF7 EGF, HRG stimulation
  • organism-icon Homo sapiens
  • sample-icon 68 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Sharing common ErbB/HER receptor signaling pathway, heregulin (HRG) induces differentiation of MCF-7 breast cancer cells while epidermal growth factor (EGF) elicits proliferation. Although the cell fate led by those two ligands was totally different, the gene expression profile in early transcription was unexpectedly qualitatively similar, suggesting that the gene expression in late transcription, not early transcription, may reflect a respect of ligand specificity. In this study, based on the data from time-course microarray of all human genes, we predicted and determined a series of transcription factors which may control HRG-specific timed-late transcription and cellular differentiation of MCF-7 cells. Validation analyses showed that one of activator protein 1 (AP-1) families appeared just after c-Fos expression, another AP-1 family partner, induced expression of another transcription factor through activation of AP-1 complex. Furthermore, expression of this transcription factors caused suppression of extracellular signal-regulated kinase (ERK) phosphorylation which is sustainedly regulated by HRG-initiated ErbB signaling. Overall, our analysis indicated an importance of formation of timed-transcriptional regulatory network and its function to control upstream signaling pathway through negative feedback for cellular differentiation.

Publication Title

Ligand-specific sequential regulation of transcription factors for differentiation of MCF-7 cells.

Sample Metadata Fields

Cell line

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accession-icon GSE25090
Gene Expression profiles of human iPS cells from CBC
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We investigated that gene expression profile of generated human iPS cells from cord blood cells using temperature sensitive sendai-virus vector.

Publication Title

Efficient generation of transgene-free human induced pluripotent stem cells (iPSCs) by temperature-sensitive Sendai virus vectors.

Sample Metadata Fields

Specimen part

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accession-icon GSE11729
H1299 EGF and Iressa stimulation
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Controlled activation of epidermal growth factor receptor (EGFR) is systematically guaranteed at the molecular level, however aberrant activation of EGFR is frequently found in cancer. Transcription induced by EGFR activation often involves coordinated expression of genes that positively and negatively regulate the original signaling pathway, therefore alterations in EGFR kinase activity may reflect changes in gene expression associated with the pathway. In this study, we investigated transcriptional changes following EGF stimulation with or without the EGFR kinase inhibitor Iressa in H1299 human non-small-cell lung cancer cells (parental H1299, H1299 cells which overexpress wild-type: EGFR-WT and mutant EGFR: L858R). Our results clearly showed differences in transcriptional activity in the absence or presence of EGFR kinase activity, and genes sharing the same molecular functions showed distinct expression dynamics. The results showed particular enrichment of EGFR/ErbB signaling-related genes in a differentially expressed gene set, and significant protein expression of MIG6/RALT(ERRFI1), an EGFR negative regulator, was confirmed in L858R. High MIG6 protein expression was correlated with basal EGFR phosphorylation and inversely correlated with EGF-induced ERK phosphorylation levels. Investigation of NCI-60 cell lines showed that ERRFI1 expression was correlated with EGFR expression regardless of tissue type. These results suggest that cells accumulate MIG6 as an inherent negative regulator to suppress excess EGFR activity when basal EGFR kinase activity is considerably high. Taken together, an EGFR mutation can cause transcriptional changes to accommodate the activation potency of the original signaling pathway at the cellular level.

Publication Title

Mutation of epidermal growth factor receptor is associated with MIG6 expression.

Sample Metadata Fields

Cell line

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accession-icon SRP135900
Transcriptomic analysis of human tonsillar TFH subsets
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We used an IL4-capture assay followed by FACS sorting, to isolate IL4-secreting TFH cells from a human tonsil and compared their transcriptomic profiles with CXCR5hi PD1hi IL4-negative tonsillar TFH cells and IL4-producing CXCR5neg non-TFH cells (TH2 cells). Our studies validate the notion of functionally distinct TFH subsets and identify genes that are specifically expressed in and define the human IL-4 secreting TFH cell subset. Overall design: T follicular helper cell subset mRNA profiles from human tonsils were generated by deep sequencing. Naive CD4 T cells, IL4-producing nonTFH CD4 T cells (i.e. TH2), and IL4-producing TFH cells and PD1hi TFH cells were analyzed. DOI: 10.26508/lsa.201800050

Publication Title

The expansion in lymphoid organs of IL-4<sup>+</sup> BATF<sup>+</sup> T follicular helper cells is linked to IgG4 class switching in vivo.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE76999
Capacity of yolk sac macrophages, fetal liver and adult monocytes to colonize an empty niche and develop into functional tissue resident macrophages
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Tissue-resident macrophages can derive from yolk sac macrophages, fetal liver monocytes or adult bone marrow monocytes. Whether these precursors can give rise to transcriptionally identical alveolar macrophages is unknown. Here, we transferred traceable yolk sac macrophages, fetal liver monocytes, adult bone marrow monocytes or adult alveolar macrophages as a control, into the empty alveolar macrophage niche of neonatal Csf2rb-/- mice. All precursors efficiently colonized the alveolar niche and generated alveolar macrophages that were transcriptionally almost identical, with only 22 genes that could be linked to their origin. Underlining the physiological relevance of our findings, all transfer-derived alveolar macrophages self-maintained within the lungs for up to 1 year and durably prevented alveolar proteinosis. Thus, precursor origin does not affect the development of functional self-maintaining tissue-resident macrophages.

Publication Title

Yolk Sac Macrophages, Fetal Liver, and Adult Monocytes Can Colonize an Empty Niche and Develop into Functional Tissue-Resident Macrophages.

Sample Metadata Fields

Specimen part

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accession-icon GSE34913
Expression data from RAW264.7 murine macrophages infected with Toxoplasma gondii and subsequently stimulated with interferon-gamma
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Toxoplasma strains are known to inhibit the expression of several interferon-gamma induced genes, and a type II strain was shown to dysregulate genome-wide responses to interferon-gamma in human fibroblasts (Kim et al., 2007, J Immunol.). In this study we aimed to determine the effect of infection with three clonal lineages of Toxoplasma, type I, II, and III strains on genome-wide interferon-gamma induced transcription in murine macrophages. We also assessed the effect of the two main Toxoplasma modulators of mouse macrophage transcription, ROP16 and GRA15 (Jensen et al., 2011, Cell Host Microbe).

Publication Title

Toxoplasma gondii clonal strains all inhibit STAT1 transcriptional activity but polymorphic effectors differentially modulate IFNγ induced gene expression and STAT1 phosphorylation.

Sample Metadata Fields

Specimen part

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accession-icon SRP023475
The genetic basis for individual differences in mRNA splicing and APOBEC1 editing activity in murine macrophages
  • organism-icon Mus musculus
  • sample-icon 111 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Alternative splicing and mRNA editing are known to contribute to transcriptome diversity. Although alternative splicing is pervasive and known to contribute to a variety of pathologies, including cancer, the genetic context for individual differences in isoform usage is still evolving. Similarly, although mRNA editing is ubiquitous and associated with important biological processes such as intracellular viral replication and cancer development, individual variations in and the genetic transmissibility of mRNA editing are equivocal. Here, we have used linkage analysis to show that both mRNA editing and alternative splicing are regulated by the macrophage genetic background and environmental cues. We show that distinct loci, potentially harboring variable splice factors, regulate the splicing of multiple transcripts. Additionally, we show that individual genetic variability at the Apobec1 locus results in differential rates of C-to-U(T) editing in murine macrophages; with mouse strains expressing mostly a truncated isoform of Apobec1 exhibiting lower rates of editing. As a proof of concept, we have used linkage analysis to identify 36 high confidence novel edited sites. These results provide a novel and complementary method that can be used to identify C-to-U editing sites in individuals segregating at specific loci and show that, beyond individual DNA sequence and structural changes, differential isoform usage and mRNA editing can contribute to intra-species genomic and phenotypic diversity. Overall design: Bone marrow derived macrophages (BMDM) from female AxB/BxA mice were left unstimulated or stimulated with IFNG/TNF, or CpG for 18 hrs or infected with infected with type II (Pru A7) for 8 hrs. The transcriptional response was then measured using the illumina RNA-seq protocol on an illumuna HiSeq 2000.

Publication Title

The genetic basis for individual differences in mRNA splicing and APOBEC1 editing activity in murine macrophages.

Sample Metadata Fields

Age, Specimen part, Cell line, Treatment, Subject

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accession-icon SRP077462
Analysis of gene expression profiles in wild-type vs Ets1-/- follicular B cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Ets1-/- mice have an increase in B cell differentiation to plasma cells and increased serum immunoglobulin levels. The genes in B cells that are transcriptionally regulated by Ets1 and help regulate B cell differentiation are largely unknown. Here, we identify Ets1-regulated target genes in B cells using ChIP-seq and RNA-seq analysis. We found that Ets1 targets genes associated with immune response, mature B cell differentiation and regulation of B cell activation. Overall design: Quiescent follicular B cells were sorted from the spleens of wild-type and Ets1-/- mice using the following markers B220+ CD23-high CD21-low CD80-negative IgA-negative IgE-negative IgG1-negative IgG2a-negative IgG2b-negative IgG3-negative. Total RNA was prepared from sorted cells and subjected to RNA-sequencing.

Publication Title

Genome-Wide Identification of Target Genes for the Key B Cell Transcription Factor <i>Ets1</i>.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE6542
Circadian time course
  • organism-icon Drosophila melanogaster
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integration of light and temperature in the regulation of circadian gene expression in Drosophila.

Sample Metadata Fields

No sample metadata fields

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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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