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accession-icon GSE55315
Progesterone Antagonist Therapy in a Pelizaeus-Merzbacher Mouse Mode
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Pelizaeus-Merzbacher disease (PMD) is a severe hypomyelinating disease, characterized by ataxia, intellectual disability, epilepsy and premature death. In the majority of cases, PMD is caused by duplication of PLP1 that is expressed in myelinating oligodendrocytes. Despite detailed knowledge of PLP1, there is presently no curative therapy for PMD. We used a Plp1 transgenic PMD mouse model to test the therapeutic effect of Lonaprisan, an antagonist of the nuclear progesterone receptor, in lowering Plp1 mRNA overexpression. We applied placebo-controlled Lonaprisan therapy to PMD mice for 10 weeks and performed the grid slip analysis to assess the clinical phenotype. Additionally, mRNA expression and protein accumulation as well as histological analysis of the central nervous system were performed. While Plp1 mRNA levels are increased about 1.8-fold in PMD mice compared to wildtype controls, daily Lonaprisan treatment reduced overexpression at the RNA level up to 1.5-fold, which was sufficient to significantly improve a poor motor phenotype. Electron microscopy confirmed a 25% increase in the number of myelinated axons in the corticospinal tract when compared to untreated PMD mice. Microarray analysis revealed the upregulation of pro-apoptotic genes in PMD mice that could be partially rescued by Lonaprisan treatment, which also reduced microgliosis, astrogliosis, and lymphocyte infiltration.

Publication Title

Progesterone antagonist therapy in a Pelizaeus-Merzbacher mouse model.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP128580
PEST-domain-enriched tyrosine phosphatase and glucocorticoids as regulators of mast cell signalling
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

PEST-domain-enriched tyrosine phosphatase (PEP) is a cytoplasmic protein tyrosine phosphatase that regulates immune cell functions, including mast cell functions. Using bone marrow derived mast cells (BMMCs) from PEP+/+ and PEP-/- mice, RNA-seq data showed that dinitrophenol (DNP) - activated PEP-/- BMMCs have misregulated gene expression, with some cytokine/chemokine genes (eg.TNFa, IL13, CSF2) showing reduced gene expression in the dinitrophenol (DNP) - activated PEP-/- BMMCs compared to (DNP)-activated PEP+/+ BMMCs. Also, the ability of the glucocorticoid dexamethasone (Dex) to negatively regulate DNP - induced COX-2 gene expression in PEP-/- BMMCs was inhibited compared to the PEP+/+ BMMCs. Overall design: Biological replicates are sequenced and analyzed. The samples are either wild-type or mutant for PEP and cells were sensitized with Ig-E, activated with Dinitrophenol and glucocorticoid treatment done with Dexamethasone.

Publication Title

Transcriptomic data on the role of PEST-domain-enriched tyrosine phosphatase in the regulation of antigen-mediated activation and antiallergic action of glucocorticoids in mast cells.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment, Subject

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accession-icon GSE9526
Expression data from cumulus cells that surround oocytes resulting in early or late cleaving embryos
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Besides the established selection criteria based on embryo morphology and blastomere number, new parameters for embryo viability are needed to improve the clinical outcome of in vitro fertilization (IVF) and more particular of elective single embryo transfer (eSET). The aim of the study was to analyse genome-wide whether the embryo viability was reflected by the expression of genes in the oocyte surrounding cumulus cells. Early cleavage (EC) was chosen as a parameter for embryo viability.

Publication Title

Differential gene expression in cumulus cells as a prognostic indicator of embryo viability: a microarray analysis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE64468
Molecular mechanism of flocculation self-recognition in yeast and its role in mating and survival
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Saccharomyces cerevisiae flocculation occurs when fermentable sugars are limiting and is therefore considered as a way to enhance the survival chance of Flo-expressing yeast cells. In this paper, the role of Flo1p in mating was demonstrated by showing that the mating efficiency, which contributes to the increased survival rate as well by generating genetic variability, is increased when cells flocculate. This was revealed by liquid growth experiments in a low shear environment and differential transcriptome analysis of FLO1 expressing cells compared to the non-flocculent wild-type cells. The results show that a floc provides a uniquely organized multicellular ultrastructure that provides a suitable microenvironment to induce and perform cell conjugation.

Publication Title

Molecular mechanism of flocculation self-recognition in yeast and its role in mating and survival.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12337
Transcriptomic analysis of PPARalpha-dependent alterations during cardiac hypertrophy
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Findings suggest that PPARalpha plays a decisive role in the development of hypertrophy, affecting the functional outcome of the heart. Unfortunately, information on the nature of PPARalpha-dependent processes in cardiac hypertrophy is fragmentary and incomplete.

Publication Title

Transcriptomic analysis of PPARalpha-dependent alterations during cardiac hypertrophy.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP056237
Analysis of bone marrow derived mast cell transcriptomes in presence or absence of SialostatinL
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Goal of this study was to compare transcriptional changes in stimulated mast cells in the absence or presence of sialostatinL Overall design: mRNA profiles of 4 weeks old mast cells (BMMC derived from C57BL/6 mice ) stimulated for 24h with ionomycin in absence or presence of tick derived sialostatinL were generated by deep sequencing using Illumina HiSeq2000

Publication Title

Tick Salivary Sialostatin L Represses the Initiation of Immune Responses by Targeting IRF4-Dependent Transcription in Murine Mast Cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6556
Expression profiling of A. thaliana wild type Columbia-0 and mutant gh3.5-1D in response to pathogen Pst DC3000(avrRpt2)
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

To reveal the underlying molecular mechanism of GH3.5 action in modulating the SA and auxin pathways, we performed transcriptional profiling of gh3.5-1D plants after infection with or without Pst DC3000(avrRpt2) on a global scale using the Affymetrix Arabidopsis ATH1 GeneChip

Publication Title

Dual regulation role of GH3.5 in salicylic acid and auxin signaling during Arabidopsis-Pseudomonas syringae interaction.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE103340
Patient-derived xenograft model identifies clinically relevant subtype-specific features of colorectal cancer
  • organism-icon Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Colorectal cancer (CRC) is a heterogeneous disease classified into four consensus molecular subtype (CMSs) with distinct biological and clinical features. This study aims to understand the value of patient-derived xenografts (PDXs) in relation to these CMSs. A total of 42 primary tumors, recurrences and metastases were used to develop PDXs. Detailed genetic analyses were performed on PDXs and corresponding patient tumors to determine relationship and PDX heterogeneity. Out of 42 tumors 22 (52%) showed successfully PDX engraftment, which was biased towards metastases and CMS1 and CMS4 tumors. Importantly, gene expression analysis revealed a clinical relevant association between an engraftment gene signature and prognosis for stage II patients. Moreover, this gene signature revealed an association between Src pathway activation and positive engraftment. Src pathway activity co-aligned with CMS4 and the levels of fibronectin in tumors and was confirmed by pSrc immunohistochemistry. From this analysis we further deduced that decreased cell cycle activity is a prognostic factor for successful engraftment and related to patient prognosis. However, this is not a general phenomenon, but subtype specific as decreased cell cycle activity was highly prognostic for recurrence-free survival within CMS2 but not in CMS1 and CMS4, while it showed an inverse correlation in CMS3. These data illustrate that CRC PDX establishment is biased toward CMS1 and CMS4, which impacts translation of results derived from pre-clinical studies using PDXs. Moreover, our analysis reveals subtype-specific features, pSrc in CMS4 and low Ki67 in CMS2, which provide novel avenues for therapy and diagnosis.

Publication Title

Capturing colorectal cancer inter-tumor heterogeneity in patient-derived xenograft (PDX) models.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE17375
Gene expression in colon cancer stem cells (CSC) cultures identified by Wnt signaling levels
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Primary colon CSC cultures were transduced with a Wnt responsive construct (TOP-GFP) and were single cell cloned. 10% highest and lowest TOP-GFP cell fractions were FACS sorted and arrayed.

Publication Title

Wnt activity defines colon cancer stem cells and is regulated by the microenvironment.

Sample Metadata Fields

Specimen part

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accession-icon SRP060710
Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

During pneumonic plague, the bacterium Yersinia pestis elicits the development of inflammatory lung lesions that continue to expand throughout infection. This lesion development and persistence is poorly understood. Here, we examine spatially distinct regions of lung lesions using laser capture microdissection and RNAseq analysis to identify transcriptional differences between lesion microenvironments. We show that cellular pathways involved in leukocyte migration and apoptosis are down regulated in the center of lung lesions compared to the periphery. Probing for the bacterial factor(s) important for the alteration in neutrophil survival, we show both in vitro and in vivo that Y. pestis increases neutrophil survival in a manner that is dependent on the type-III secretion system effector YopM. This research explores the complexity of spatially distinct host - microbe interactions and emphasizes the importance of cell relevance in assays in order to fully understand Y. pestis virulence. Overall design: We examine spatially distinct regions of lung lesions using laser capture microdissection and RNAseq analysis to identify transcriptional differences between lesion microenvironments. Sample types: uninfected BM-PMN, infected BM-PMN, lesion periphery, lesion center.

Publication Title

Spatially distinct neutrophil responses within the inflammatory lesions of pneumonic plague.

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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