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accession-icon SRP035393
Widespread inhibition of post-transcriptional splicing shapes the cellular transcriptome following heat shock
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Heat shock timecourse RNAseq, 3T3 cells

Publication Title

Widespread inhibition of posttranscriptional splicing shapes the cellular transcriptome following heat shock.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP107191
Comparative analysis reveals genomic features of stress-induced transcriptional readthrough
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcription is a highly regulated process, and stress-induced changes in gene transcription have been shown to play a major role in responses and adaptation to stress. Numerous emerging genome-wide studies reveal prevalent transcription beyond known protein-coding gene loci, generating a variety of new classes of RNAs, most of unknown function. One such class, termed downstream of gene (DoG)-containing transcripts, was reported to result from transcriptional readthrough upon osmotic stress in human cell lines. However, how widespread the readthrough phenomenon is, and what its causes and consequences are, remain elusive. Here we present a systematic genome-wide mapping of transcriptional readthrough, using deep nuclear RNA-seq, comparing heat shock, osmotic and oxidative stress in NIH3T3 mouse fibroblast cells. We observe massive induction of transcriptional readthrough under all stress conditions, with significant, yet not complete overlap of readthrough-induced loci between different conditions. Importantly, our analyses suggest that stress-induced transcriptional readthrough is not a random failure process, but is rather differentially induced across different conditions. Additionally, analyzing public Pol-II occupancy data further supported our findings of stress-induced readthrough. We explore potential regulators and find a role for HSF1 in the induction of a subset of heat shock-induced readthrough transcripts. Furthermore, we examine genomic features of readthrough transcription, and observe a unique chromatin signature typical of DoG-producing regions, suggesting that readthrough transcription is associated with the maintenance of an open chromatin state. Overall design: RNA profiles of NIH3T3 (mouse embryonic fibroblasts) cells after three stress treatments and control were generated by deep sequencing, in two replicates using Illumina HiSeq 2000.

Publication Title

Comparative analysis reveals genomic features of stress-induced transcriptional readthrough.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE24986
Response of A549 cells treated with Aspergillus fumigatus
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE24984
Response of A549 cells treated with Aspergillus fumigatus [WT-GC_vs_PrtT-GC]
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Response of A549 cells treated with Aspergillus fumigatus wild type germinating conidia (WT_GC) or PrtT protease deficient mutant conidia (PrtT-GC) or inert acrylic 2-4 micron beads (Beads) for 8h

Publication Title

PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE24985
Response of A549 cells treated with Aspergillus fumigatus [WT-CF_vs_PrtT-CF]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Response of A549 cells treated with Aspergillus fumigatus wild type culture filtrate (WT-CF) or PrtT protease deficient mutant culture filtrate (PrtT-CF) for 8h

Publication Title

PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE24983
Response of A549 cells treated with Aspergillus fumigatus [WT-CF_vs_WT-GC]
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Response of A549 cells treated with Aspergillus fumigatus germinating conidia (WT-GC) or culture filtrate (WT-CF) for 8h

Publication Title

PrtT-regulated proteins secreted by Aspergillus fumigatus activate MAPK signaling in exposed A549 lung cells leading to necrotic cell death.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE28044
Expression data from non-malignant fallopian tube epithelium
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarrays were used to examine gene expression changes that may be present in the fallopian tube epithelium of morphologically normal BRCA1 mutation positive and negative subjects. Fallopian tube epithelia has been implicated as an early point of origin for serous carcninoma. By examining the early events present in the microenvironment of this tissue between BRCA1 mutation carriers and non-carriers, we hoped to elucidate mechanisms that may lead to the development of epithelial ovarian cancer.

Publication Title

Identification of abrogated pathways in fallopian tube epithelium from BRCA1 mutation carriers.

Sample Metadata Fields

Specimen part

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accession-icon SRP048798
Transcription factor Oct1 and its coactivator OCA-B are selectively required for CD4 memory T cell formation and function
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Epigenetic changes are crucial for the generation of immunological memory1-4. Failure to generate or maintain these changes will result in poor memory responses. Similarly, augmenting or stabilizing the correct epigenetic states offers a potential method of enhancing immune memory. Yet the transcription factors that regulate these processes are poorly defined, as are the chromatin modifying complexes they recruit and the chromatin modifications they control. Using pathogen infection models and three different mouse models, including a new conditional allele, we find that the widely expressed transcription factor Oct15, and its cofactor OCA-B6,7, are selectively required the in vivo generation of functional CD4 memory. In vitro, both proteins are also required to maintain a poised state at the Il2 target locus in resting but previously stimulated CD4 T cells, and to generate robust Il2 expression upon restimulation. OCA-B is also required for the robust re-expression of other known targets including Il17a, and Ifng. We identify an underlying mechanism involving OCA-B recruitment of the histone lysine demethylase Jmjd1a8 to targets such as Il2 and Ifng. The findings pinpoint Oct1 and OCA-B as unanticipated mediators of CD4 T cell memory. Overall design: Examination of 4 different conditions in 2 genotypes

Publication Title

Oct1 and OCA-B are selectively required for CD4 memory T cell function.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE72359
p53 amplifies Toll-like receptor 5 response in MCF-7 cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Using gene expression profiling we characterize the global effect of p53 on the TLR5-mediated transcription in MCF7 cells. We found that combined activation of p53 and TLR5 pathways synergistically increases expression of over 200 genes, mostly associated with immunity and inflammation. The synergy was observed in several human cancer cells and primary lymphocytes.

Publication Title

p53 amplifies Toll-like receptor 5 response in human primary and cancer cells through interaction with multiple signal transduction pathways.

Sample Metadata Fields

Cell line

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accession-icon GSE11917
Vitamin D sterol effects on coronary ASMC genes
  • organism-icon Homo sapiens
  • sample-icon 102 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Chondro/osteoblastic and cardiovascular-disease associated genes are modulated in human coronary artery smooth muscle cells that calcify in the presence of phosphate and vitamin D sterols.

Publication Title

Chondro/osteoblastic and cardiovascular gene modulation in human artery smooth muscle cells that calcify in the presence of phosphate and calcitriol or paricalcitol.

Sample Metadata Fields

No sample metadata fields

View Samples
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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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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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