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accession-icon GSE94074
Expression data of Hematopoietic progenitor and stem cells after 18h of culture with or without extracellular vesicles secreted by AFT stromal cells
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Hematopoietic progenitor and stem cells from bone marrow have been sorted by FACS (LSK, Lineage -, Sca1 + and cKit +) and co-culture during 18h without cytokines with or without extracellular vesicles (EV) secreted by AFT stromal cells.

Publication Title

Extracellular vesicles of stromal origin target and support hematopoietic stem and progenitor cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE20188
Expression data in response to neonicotinoid insecticides
  • organism-icon Arabidopsis thaliana
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Neonicotinoid insecticides control crop pests based on their action as agonists at the insect nicotinic acetylcholine receptor which accepts chloropyridinyl- and chlorothiazolyl- analogs almost equally well. In some cases, these compounds have also been reported to enhance plant vigor and (a)biotic stress tolerance, independent of their insecticidal function. However, this mode of action has not been specifically defined. Using Arabidopsis thaliana, we show that the neonicotinoid compounds, imidacloprid (IMI) and clothianidin (CLO), via their 6-chloropyridinyl-3-carboxylic acid and 2-chlorothiazolyl-5-carboxylic acid metabolites, respectively, induce salicylic acid (SA) associated plant responses. SA is a phytohormone best known for its role in plant defense against pathogens and as an inducer of systemic acquired resistance; however, it can also modulate abiotic stress responses. These neonicotinoids effect a similar global transcriptional response to that of SA including genes involved in (a)biotic stress response. Furthermore, similar to SA, IMI and CLO induce systemic acquired resistance resulting in reduced growth of a powdery mildew pathogen. The action of CLO induces the endogenous synthesis of SA via the SA biosynthetic enzyme ICS1, with ICS1 required for CLO-induced accumulation of SA, expression of the SA marker PR1, and fully enhanced resistance to powdery mildew. In contrast, the action of IMI does not induce endogenous synthesis of SA. Instead, IMI is further bioactivated to 6-chloro-2-hydroxypyridinyl-3-carboxylic acid, which is shown here to be a potent inducer of PR1 and inhibitor of SA-sensitive enzymes. Thus, via different mechanisms, these chloropyridinyl- and chlorothiazolyl- neonicotinoids induce SA responses associated with enhanced stress tolerance.

Publication Title

Neonicotinoid insecticides induce salicylate-associated plant defense responses.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE37209
Expression data from Paneth cells isolated from mice on calorie restricted or ad libitum diet
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Paneth cells recide in the intestinal crypt bottom and are part of the innate immunity and of the intestinal stem cell niche.

Publication Title

mTORC1 in the Paneth cell niche couples intestinal stem-cell function to calorie intake.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP127409
4 NSCLC cell lines treated with GDC-0973, AZ-628 or a combination of both
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

RNA was purified cancer cell lines. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is PRJ0013114 Overall design: RNA from NSCLC cell lines after treatment with either DMSO, GDC-0973, AZ-628 or the combination of AZ-628 and GDC-0973 all at 0.1 micro-molar concentration.

Publication Title

Pharmacological Induction of RAS-GTP Confers RAF Inhibitor Sensitivity in KRAS Mutant Tumors.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE19655
Reprogramming of anaerobic metabolism by the FnrS Small RNA
  • organism-icon Escherichia coli
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Small RNAs (sRNA) that act by base pairing with trans-encoded mRNAs modulate metabolism in response to a variety of environmental stimuli. Here, we describe an Hfq-binding sRNA (FnrS) whose expression is induced upon a shift from aerobic to anaerobic conditions and which acts to down regulate the levels of a variety of mRNAs encoding metabolic enzymes. Anaerobic induction in minimal medium depends strongly on FNR but is also affected by ArcA and CRP. Whole genome expression analysis showed that the levels of at least 32 mRNAs are down regulated upon FnrS overexpression, 15 of which are predicted to base pair with FnrS by TargetRNA. The sRNA is highly conserved across its entire length in numerous enterobacteria, and mutation analysis revealed that two separate regions of FnrS base pair with different sets of target mRNAs. The majority of the target genes previously reported to be down regulated in an FNR-dependent manner lack recognizable FNR binding sites. We thus suggest that FnrS extends the FNR regulon and increases the efficiency of anaerobic metabolism by repressing the synthesis of enzymes that are not needed under these conditions.

Publication Title

Reprogramming of anaerobic metabolism by the FnrS small RNA.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE18517
Gene expression profiling in Al-tolerant and Al-sensitive soybean under aluminum stress
  • organism-icon Glycine max
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

Gene expression profiling in soybean under aluminum stress: genes differentially expressed between Al-tolerant and Al-sensitive genotypes.

Publication Title

Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE18518
Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity
  • organism-icon Glycine max
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level.

Publication Title

Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE18423
Soybean transcriptome response to aluminum stress in roots of Al-tolerant genotype (PI 416937): time course
  • organism-icon Glycine max
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Soybean Genome Array (soybean)

Description

Gene expression profiling in soybean under aluminum stress: Transcriptome response to Al stress in roots of Al-tolerant genotype (PI 416937).

Publication Title

Identification of Aluminum Responsive Genes in Al-Tolerant Soybean Line PI 416937.

Sample Metadata Fields

Specimen part

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accession-icon GSE76072
Genome wide mapping of NR4A binding reveals cooperativity with ETS factors to promote epigenetic activation of distal enhancers in acute myeloid leukemia cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome Wide Mapping of NR4A Binding Reveals Cooperativity with ETS Factors to Promote Epigenetic Activation of Distal Enhancers in Acute Myeloid Leukemia Cells.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE79490
Genome wide mapping of NR4A binding reveals cooperativity with ETS factors to promote epigenetic activation of distal enhancers in acute myeloid leukemia cells [array]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

NR4As are critical tumor suppressors of acute myeloid leukemia (AML) whose expression is broadly silenced in leukemia initiating cell enriched populations from human patients relative to normal hematopoietic stem/progenitor cells. Rescued NR4A expression in human AML cells inhibits proliferation and reprograms AML gene signatures via transcriptional mechanisms that remain to be elucidated. By intersecting an acutely regulated, NR4A1 dependent transcriptional profile with genome wide NR4A binding distribution, we now identify an NR4A targetome of 685 genes that are directly regulated by NR4A1. We show that NR4As regulate gene transcription primarily through interaction with distal enhancers that are co-enriched for both NR4A1 and ETS transcription factor motifs. Using a subset of NR4A activated genes, we demonstrate that the ETS factors ERG and FLI-1 are required for activation of NR4A bound enhancers and NR4A target gene induction. NR4A1 dependent recruitment of ERG and FLI-1 promotes binding of p300 histone acetyl transferase to activate NR4A bound enhancers. These findings disclose novel epigenetic mechanisms by which NR4As and ETS factors cooperate to drive NR4A dependent gene transcription in human AML cells.

Publication Title

Genome Wide Mapping of NR4A Binding Reveals Cooperativity with ETS Factors to Promote Epigenetic Activation of Distal Enhancers in Acute Myeloid Leukemia Cells.

Sample Metadata Fields

Cell line, Treatment

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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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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