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accession-icon GSE69058
Gene expression data from mouse tracheal cells before and 48hrs after SO2 injury
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE69056
Gene expression data from mouse tracheal epithelial cells isolated before and 48hrs after SO2 injury
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The conducting airway epithelium of the rodent and human lung is made up of about equal proportions of ciliated and secretory cells. In addition, in regions where the epithelium is pseudostratfied, ~30% of the epithelium consists of undifferentiated basal cells (BCs). Evidence suggests that these BCs are multipotent stem cells that can self renew over the long term and give rise to both ciliated and secretory lineages. The goal of this project is to identify cellular and molecular mechanisms by which the basal cells normally maintain the epithelium and repair it after injury.

Publication Title

BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE69057
Gene expression data from mouse tracheal mesenchymal cells before and 48hrs after SO2 injury
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The conducting airway epithelium of the rodent and human lung is underlaid by mesenchymal cells that include vasculature, smooth muscle, fibroblasts and cartilage. The goal of this project is to identify cellular and molecular changes in the mesenchyme after injury to the epithelium by exposure to SO2 and which may participate in repair of the epithelium

Publication Title

BMP signaling and cellular dynamics during regeneration of airway epithelium from basal progenitors.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE16963
Induction of pluripotent stem cells from human third molar mesenchymal stromal cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The expression of four transcription factors (OCT3/4, SOX2, KLF4, and c-MYC) can reprogram mouse as well as human somatic cells to induced pluripotent stem (iPS) cells. Expression of the c-MYC, also known as an oncogene, might induce carcinogenesis and thus, iPS cells produced with the use of c-MYC transduction cannot be used for human therapeutic applications. Furthermore, reprogramming efficiency was significantly reduced in the absence of c-MYC transduction. Here, we generated iPS cells from mesenchymal stromal cells (MSCs) derived from human third molars (wisdom teeth) by retroviral transduction of OCT3/4, SOX2, and KLF4 without c-MYC. Interestingly, clonally expanded MSCs, named 10F-15, could be used for iPS cell generation with 100-fold higher efficiency compared to that of other clonally expanded MSCs and human dermal fibroblasts. These iPS cells resembled human embryonic stem (ES) cells in many aspects, including morphology, ES markers expression, global gene expression, epigenetic states, and the ability to differentiate into the three germ layers in vitro and in vivo. Because human third molars are discarded as clinical waste, our data indicate that MSCs isolated from human third molars are a valuable cell source for the generation of iPS cells.

Publication Title

Induction of pluripotent stem cells from human third molar mesenchymal stromal cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE48237
Innate and antigen-specific cytotoxic cells and Paradoxical HIV-associated Tuberculosis Immune reconstitution inflammatory syndrome (TB-IRIS)
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Tuberculosis Immune Reconstitution Inflammatory Syndrome (TB-IRIS) frequently complicates combined anti-retroviral therapy (ART) and anti-tubercular therapy in HIV-1 co-infected tuberculosis (TB) patients. The immunopathological mechanism underlying TB-IRIS is incompletely defined.

Publication Title

Cytotoxic mediators in paradoxical HIV-tuberculosis immune reconstitution inflammatory syndrome.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP162249
ALS/FTD-linked mutation in FUS suppresses intra-axonal protein synthesis and drives disease without nuclear loss-of-function of FUS
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Through the generation of humanized FUS mice expressing full length human FUS, we identify that when expressed at near endogenous murine FUS levels both wild-type or ALS- and frontotemporal dementia (FTD)-causing mutations complement the essential function(s) of murine FUS. Replacement of murine FUS with mutant, but not wild-type, human FUS causes stress-mediated induction of chaperones, decreased expression of ion channels/transporters essential for synaptic function, and reduced synaptic activity, without loss of nuclear FUS or its cytoplasmic aggregation. Most strikingly, accumulation of mutant human FUS is shown to activate an integrated stress response and inhibit local, intra-axonal protein synthesis in hippocampal neurons and sciatic nerves. Collectively, our evidence demonstrates that human ALS/FTD-linked mutations in FUS induce a gain-of-toxicity that includes stress-mediated suppression in intra-axonal translation, synaptic dysfunction, and progressive, age-dependent motor and cognitive disease without cytoplasmic aggregation, altered nuclear localization, or aberrant splicing of FUS-bound pre-mRNAs. Methods: RNA from mouse spinal cords of 18-month-old mFUS-/-/hgFUS (WT, R521C or R521H) and their Non-Tg control littermates was extracted with TRIzol. RNA quality was measured using the Agilent Bioanalyzer system and processed using the Illumina TruSeq Stranded mRNA Sample Preparation Kit according to manufacturer's protocols. mRNA profiles were generated by deep sequencing, with n=3 biological replicates per group. Results: We mapped on average 15 million non-redundant reads per sample. Fastq files were aligned to mouse reference genome (mm9 UCSC Genome Browser) using TopHat workfow and the transcript abundance for each annotated protein-coding gene [as fragments per kilobase of transcript per million mapped reads (FPKM)] was estimated by Cufflinks. 13,468 genes which expressed FPKM>=1 were kept for downstream analyses. RNA profiles from normal (Non-Tg) and humanized hgFUSWT mice were almost undistinguishable. Both humanized mutant FUS lines had highly distinct RNA profiles [determined with unsupervised hierarchical clustering and principal component analysis (PCA)], with 709 down and 348 up-regulated genes relative to age-matched Non-Tg or humanized hgFUSWT littermates (P<0.05). These changes uncovered FUS mutant dependent altered pathways that may contribute to ALS/FTD-linked mutant FUS-mediated toxicity. The validation by RT-QPCR of altered expression of 20 genes is shown in Figure 5. Overall design: RNA expression profile of mouse spinal cords from 18-month-old mFUS-/-/hgFUS (WT, R521C or R521H) and their Non-Tg control littermates was obtained by deep sequencing in n=3 indendepent animals per genotype using Illumina HiSeq 2000 sequencer.

Publication Title

ALS/FTD-Linked Mutation in FUS Suppresses Intra-axonal Protein Synthesis and Drives Disease Without Nuclear Loss-of-Function of FUS.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE10345
Genome-wide analysis of transcriptional termination in E. coli
  • organism-icon Escherichia coli
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Transcription termination factor Rho is essential in enterobacteria. We inhibited Rho activity with bicyclomycin and used microarray experiments to assess Rho function on a genome-wide scale. Rho is a global regulator of gene expression that matches E. coli transcription to translational needs. Remarkably, genes that are most repressed by Rho are prophages and other horizontally-acquired portions of the genome. Elimination of these foreign DNA elements increases resistance to bicyclomycin. Although rho remains essential, such reduced-genome bacteria no longer require Rho cofactors NusA and NusG. Thus, Rho termination, supported by NusA and NusG, is required to suppress the toxic activity of foreign DNA.

Publication Title

Termination factor Rho and its cofactors NusA and NusG silence foreign DNA in E. coli.

Sample Metadata Fields

Compound

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accession-icon SRP188242
RNA-seq analyses of human prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To study the transcriptome of human prostate cancer cells, RNA-seq experiments were performed. Overall design: RNA was harvested after 72h of steroid deprivation to study the basal transcriptome of LNCaP and 22rv1 cells, two human AR-positive prostate cancer cell lines,

Publication Title

Reprogramming of Isocitrate Dehydrogenases Expression and Activity by the Androgen Receptor in Prostate Cancer.

Sample Metadata Fields

Subject

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accession-icon GSE34047
SA, elf18 treatment of WT and tbf1 mutant
  • organism-icon Arabidopsis thaliana
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Identification of TBF1-dependent and SA, elf18-responsive genes in Arabidopsis

Publication Title

The HSF-like transcription factor TBF1 is a major molecular switch for plant growth-to-defense transition.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE22274
H. arabidopsidis EMWA1 infection, time course experiment
  • organism-icon Arabidopsis thaliana
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

We used microarrays to identify differentially expressed genes. We focused on those genes that were dramatically induced (>2-fold) in WT but not in the rpp4 mutant at 2 dpi when WT and rpp4 first showed distinct phenotypes

Publication Title

Timing of plant immune responses by a central circadian regulator.

Sample Metadata Fields

Specimen part, Time

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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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