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accession-icon GSE40466
Expression profiling of TGF-beta-induced and hnRNP E1-mediated epithelial-mesenchymal transition
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Regulation of gene expression at the post-transcriptional level plays an indispensable role during TGFbeta-induced EMT and metastasis. This regulation involves a transcript-selective translational regulatory pathway in which a ribonucleoprotein (mRNP) complex, consisting of heterogeneous nuclear ribonucleoprotein E1 (hnRNP E1) and eukaryotic elongation factor 1A1 (eEF1A1), binds to a 3-UTR regulatory BAT (TGF activated translation) element and silences translation of Dab2 and ILEI mRNAs, two transcripts which are involved in mediating EMT. TGFbeta activates a kinase cascade terminating in the phosphorylation of hnRNP E1, by isoform-specific stimulation of protein kinase B/Akt2, inducing the release of the mRNP complex from the 3-UTR element, resulting in the reversal of translational silencing and increased expression of Dab2 and ILEI transcripts.

Publication Title

Establishment of a TGFβ-induced post-transcriptional EMT gene signature.

Sample Metadata Fields

Specimen part

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accession-icon GSE79809
Differential production of Type I IFN determines the reciprocal levels of IL-10 and proinflammatory cytokines produced by C57BL/6 and BALB/c macrophages
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Pattern recognition receptors (PRR) detect microbial products and induce cytokines which shape the immunological response. Interleukin-12 (IL-12), tumor necrosis factor alpha (TNF-) and IL-1 are proinflammatory cytokines which can be essential for resistance against infection, but if produced at high levels, may contribute to immunopathology. In contrast, IL-10 is an immunosuppressive cytokine which dampens proinflammatory responses, but can also lead to defective pathogen clearance. The regulation of these cytokines is therefore central to the generation of an effective but balanced immune response. Here, we show that macrophages derived from C57BL/6 mice produce low levels of IL-12, TNF- and IL-1, but high levels of IL-10 in response to TLR4 and TLR2 ligands LPS and PamCSK4, and Burkholderia pseudomallei a Gram-negative bacterium which activates TLR 2/4. In contrast, macrophages derived from BALB/c mice show a reciprocal pattern of cytokine production. Differential production of IL-10 in B. pseudomallei and LPS stimulated C57BL/6 and BALB/c macrophages was due to a type I IFN dependent, but IL-27 independent mechanism. Further, type I IFN contributed to differential IL-1 and IL-12 production in B. pseudomallei and LPS stimulated C57BL/6 and BALB/c macrophages, via both IL-10-dependent and independent mechanisms. These findings highlight key pathways responsible for the regulation of pro- and anti-inflammatory cytokines in macrophages and reveal how they may differ according to the genetic background of the host.

Publication Title

Differential Production of Type I IFN Determines the Reciprocal Levels of IL-10 and Proinflammatory Cytokines Produced by C57BL/6 and BALB/c Macrophages.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

View Samples
accession-icon GSE77102
Analysis of transcriptional signatures in response to Listeria monocytogenes infection reveals temporal and strain dependent changes in interferon signalling
  • organism-icon Mus musculus
  • sample-icon 192 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Listeriosis is an infectious disease caused by the intracellular bacterium Listeria monocytogenes. To control the infection effectively, the host immune response is directed by intercellular signalling molecules called cytokines that are produced by immune cells following sensing of the bacteria. In this study we used gene expression analysis to examine complex immune signalling networks in the blood and tissues of mice infected with L. monocytogenes. We show that a large set of genes are perturbed in both blood and tissue upon infection and that the transcriptional responses in both are enriched for pathways of the immune response. From these data we also observe an important signalling network emerge from a group of cytokines called interferons (IFNs). Previous findings suggest that different IFN family members can determine the balance between successful and impaired immune responses to L. monocytogenes and several other bacterial infections. Using mice deficient for the detrimental type I IFN signalling pathway we show that IFN-inducible genes are differentially regulated at different times upon infection but also present at much lower levels in uninfected mice highlighting how dysregulation of this network in the steady state may determine the outcome of this bacterial infection.

Publication Title

Analysis of Transcriptional Signatures in Response to Listeria monocytogenes Infection Reveals Temporal Changes That Result from Type I Interferon Signaling.

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE28701
Transcript-level responses of Plasmodium falciparum to thiostrepton
  • organism-icon Plasmodium falciparum
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)

Description

Abstract: The antimalarial activity of the antibiotic thiostrepton has long been attributed to inhibition of apicoplast protein synthesis through binding of apicoplast ribosomal RNA. However, the kinetics of parasite death upon thiostrepton treatment differ from those seen for other inhibitors of apicoplast housekeeping functions. We have analysed global changes in gene expression of the malaria parasite, Plasmodium falciparum, in an attempt to shed light on the responses of the parasite to this drug. Our results indicate a delay in gene expression profiles of thiostrepton-treated parasites. A small number of genes appear to be regulated outside of this trend; our data suggest a response from genes encoding components of the mitochondrial translational machinery, while little response is seen from genes encoding apicoplast-targeted proteins. Our findings are consistent with an effect of thiostrepton on mitochondrial protein synthesis, and thus warrant a re-evaluation of the target of thiostrepton in Plasmodium. They also provide some suggestion of mitochondrion nucleus signalling in the parasite.

Publication Title

Transcript-level responses of Plasmodium falciparum to thiostrepton.

Sample Metadata Fields

Treatment

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accession-icon GSE41802
Isocitrata Dehydrogenase (IDH) Mutations Promote a Reversible ZEB1/mir-200-Dependent Epithelial Mesenchymal Transition (EMT)
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mutations in the genes encoding isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in a variety of tumor types, resulting in production of the proposed oncometabolite, 2-hydroxyglutarate (2-HG). How mutant IDH and 2-HG alter signaling pathways to promote cancer, though, remains unclear. Additionally, there exist relatively few cell lines with IDH mutations. To examine the effect of endogenous IDH mutations and 2-HG, we created a panel of isogenic epithelial cell lines with either wild-type IDH1/2 or clinically relevant IDH1/2 mutations. Differences were noted in the ability of IDH mutations to cause robust 2-HG accumulation. IDH1/2 mutants that produce high levels of 2-HG cause an epithelial-mesenchymal transition (EMT)-like phenotype, characterized by changes in EMT-related gene expression and cellular morphology. 2-HG is sufficient to recapitulate aspects of this phenotype in the absence of an IDH mutation. In the cells types examined, mutant IDH-induced EMT is dependent on upregulation of the transcription factor ZEB1 and downregulation of the mir-200 family of microRNAs. Furthermore, sustained knockdown of IDH1 in IDH1 R132H mutant cells is sufficient to reverse many characteristics of EMT, demonstrating that continued expression of mutant IDH is required to maintain this phenotype. These results suggest mutant IDH proteins can reversibly deregulate discrete signaling pathways that contribute to tumorigenesis

Publication Title

Isocitrate dehydrogenase (IDH) mutations promote a reversible ZEB1/microRNA (miR)-200-dependent epithelial-mesenchymal transition (EMT).

Sample Metadata Fields

Cell line

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accession-icon GSE25332
Restoring miR-200c to aggressive endometrial cancer cell line
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Using a mimic miR-200c was restored to an aggressive, Type 2 endometrial cancer cell line, Hec50

Publication Title

MicroRNA-200c mitigates invasiveness and restores sensitivity to microtubule-targeting chemotherapeutic agents.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE17929
Expression data from rat (Sprague Dawley) brain subjected to MCAo.
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke.

Publication Title

A secretory phospholipase A2-mediated neuroprotection and anti-apoptosis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE13109
Effect of hypoxia on gene expression in Grey poplar
  • organism-icon Populus tremula x populus alba
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Poplar Genome Array (poplar)

Description

The molecular responses of Grey poplar (Populus x canescens) following root hypoxia were studied in roots and leaves using transcript profiling. Grey poplar is a flooding tolerant tree species and analysis of the molecular response to hypoxia may indicate possible adaptation mechanisms to this stress.

Publication Title

Differential response of gray poplar leaves and roots underpins stress adaptation during hypoxia.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP041507
Fine kinetic transcriptome analysis during jasmonate signaling
  • organism-icon Arabidopsis thaliana
  • sample-icon 72 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To study the role of the plant hormone jasmonate in regulating stress-induced allocation of photosynthetic products between growth- and defense-related processes, we used RNA-sequencing to query the Arabidopsis transcriptome at high temporal resolution over 24 h after treatment with the bacterial toxin coronatine (COR), a high-affinity agonist of the JA receptor, or with a mock solution to account for diurnal changes in gene expression. These data establish a fine-scale view of the kinetics of jasmonate signaling, as well as of the diurnal patterns of gene expression.

Publication Title

Temporal Dynamics of Growth and Photosynthesis Suppression in Response to Jasmonate Signaling.

Sample Metadata Fields

Age, Specimen part, Treatment, Time

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accession-icon GSE9795
Monocular Visual Deprivation in Macaque Monkeys: A Profile in the Gene Expression of the LGN by LCM
  • organism-icon Macaca mulatta
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Rhesus Macaque Genome Array (rhesus)

Description

Laser capture microdissection was used to obtain individual LGN layers for DNA microarray of Rhesus array in macaque monkeys that Monocular Visual Deprivation was generated by either opaque dark contact lens or tarsoraphoplasty at birth.

Publication Title

Monocular visual deprivation in macaque monkeys: a profile in the gene expression of lateral geniculate nucleus by laser capture microdissection.

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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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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