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accession-icon SRP076238
alphaT-catenin in restricted brain cell types and its potential connection to autism
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-seq analysis was performed between WT and alphaT-cat KO mouse cerebella aiming to discover gene transcripts altered by the loss of alphaT-cat These altered gene transcripts could be associated with several neurologic disease-relevant pathways Overall design: Total RNA extracted of cerebellar tissue (n=3) from the brains of WT ad alphaT-cat KO mice

Publication Title

αT-catenin in restricted brain cell types and its potential connection to autism.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE40713
Mammary Gland Morphology and Gene Expression Signature of Prepubertal Male and Female Rats Following Exposure to Exogenous Estradiol
  • organism-icon Rattus norvegicus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

In order to properly understand whether xenoestrogens act as estrogens, it is essential to possess a solid portrait of the physiological effects of exogenous estradiol. Because the estrogen-dependent gene expression is one of the primary biomarkers of estrogenic action, we have assessed effects of three doses of exogenous estradiol (0.1, 1.0 and 10 g/kg of body weight/day) on the mammary gland morphology and gene expression profiles by microarray analysis of prepubertal male and female rats of both sexes compared to untreated controls. Estradiol was administered subcutaneously with minipumps from weaning at PND21 to the end of the experiment at PND33. The data suggest that the male mammary is a sensitive tissue for estrogenicity assessment.

Publication Title

Mammary gland morphology and gene expression signature of weanling male and female rats following exposure to exogenous estradiol.

Sample Metadata Fields

Sex

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accession-icon SRP156476
Identification of the genes under the control of the transcription factor Prdm12 in somatosensory neurons
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Prdm12, a novel key regulator of the Nerve Growth Factor-TrkA signaling pathway, is required for nociceptive sensory neuron development Overall design: RNA-seq analysis in triplcate of the transcriptome of thoracic dorsal root ganglia with associated spinal cord of E11.5 Prdm12 KO and WT embryos.

Publication Title

Prdm12 Directs Nociceptive Sensory Neuron Development by Regulating the Expression of the NGF Receptor TrkA.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE141253
Development of a neural rosette formation assay (RoFA) to identify neurodevelopmental toxicants and to characterize their transcriptome disturbances
  • organism-icon Homo sapiens
  • sample-icon 148 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The first in vitro tests for developmental toxicity made use of rodent cells. Newer teratology tests, e.g. developed during the ESNATS project, use human cells and measure mechanistic endpoints (such as transcriptome changes). However, the toxicological implications of mechanistic parameters are hard to judge, without functional/morphological endpoints. To address this issue, we developed a new version of the human stem cell-based test STOP-tox(UKN). For this purpose, the capacity of the cells to self-organize to neural rosettes was assessed as functional endpoint: pluripotent stem cells were allowed to differentiate to neuroepithelial cells for six days in the presence or absence of toxicants. Then, both transcriptome changes were measured (standard STOP-tox(UKN)), and cells were allowed to form rosettes. After optimization of staining methods, an imaging algorithm for rosette quantification was implemented and used for an automated rosette formation assay (RoFA). Neural tube toxicants (like valproic acid), which are known to disturb human development at stages when rosette-forming cells are present, were used as positive controls. Established toxicants led to distinctly different tissue organization and differentiation stages. RoFA outcome and transcript changes largely correlated concerning (i) the concentration-dependence, (ii) the time-dependence, and (iii) the set of positive hits identified amongst 24 potential toxicants. Using such comparative data, a prediction model for the RoFA was developed. The comparative analysis was also used to identify gene dysregulations that are particularly predictive for disturbed rosette formation. This ‘RoFA predictor gene set’ may be used for a simplified and less costly setup of the STOP-tox(UKN) assay.

Publication Title

Development of a neural rosette formation assay (RoFA) to identify neurodevelopmental toxicants and to characterize their transcriptome disturbances.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment

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accession-icon SRP170939
Antagonizing increased miR-135a levels at the chronic stage of experimental TLE reduces spontaneous recurrent seizures
  • organism-icon Mus musculus
  • sample-icon 168 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Increased miR-135a levels are observed in human patients with temporal lobe Epilepsy (TLE) and in experimental animal models. Upon targeting the increased miR-135a levels in vivo using antagomirs in kainic acid induced status epilepticus mouse model of TLE, we observed a strong reduction of spontaneous recurrent seizures. To understand this further and to find target mRNAs that potentially mediate the seizure suppressive function of miR-135a, we performed immunoprecipitation using biotin tagged miRNA mimics, followed by RNAsequencing (RNAseq). We found several novel neuronal targets of miRNA-135a and identified Mef2a as a key target in this study. Here we report the total RNAseq data. Overall design: N2A cells were transfected with biotin tagged miRNA mimics for miR-135a and negative control and immunoprecipitations were performed. N = 3 replicates of IP and input samples for each condition were generated and sequenced on illumina platform for total RNA for identification of novel targets of miR-135a.

Publication Title

Antagonizing Increased <i>miR-135a</i> Levels at the Chronic Stage of Experimental TLE Reduces Spontaneous Recurrent Seizures.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE71127
A transcriptome-based classifier to identify developmental toxicants by stem cell testing: design, validation, and optimization for histone deacetylase inhibitors
  • organism-icon Homo sapiens
  • sample-icon 82 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Test systems to identify developmental toxicants are urgently needed. A combination of human stem cell technology and transcriptome analysis was used here to provide proof-of-concept that toxicants with a related mode of action can be identified, and grouped for read-across. We chose a test system of developmental toxicity, related to the generation of neuroectoderm from pluripotent stem cells (UKN1), and exposed cells for six days to benchmark concentration (BMC) of histone deacetylase inhibitors (HDACi) valproic acid, trichostatin-A, vorinostat, belinostat, panobinostat and entinostat. To provide insight into their toxic action, we identified HDACi consensus genes, assigned them to superordinate biological processes, and mapped them to a human transcription factor network constructed from hundreds of transcriptome data sets. We also tested a heterogeneous group of mercurials (methylmercury, thimerosal, mercury(II)chloride, mercury(II)bromide, 4-chloromercuribenzoic acid, phenylmercuric acid) (BMCs). Microarray data were compared at the highest non-cytotoxic concentration for all 12 toxicants. A support vector machine (SVM)-based classifier predicted all HDACi correctly. For validation, the classifier was applied to legacy data sets of HDACi, and for each exposure situation, the SVM predictions correlated with the developmental toxicity. Finally, optimization of the classifier based on 100 probe sets showed that eight genes (F2RL2, TFAP2B, EDNRA, FOXD3, SIX3, MT1E, ETS1, LHX2) are sufficient to separate HDACi from mercurials. Our data demonstrate, how human stem cells and transcriptome analysis can be combined for mechanistic grouping and prediction of toxicants. Extension of this concept to mechanisms beyond HDACi would allow prediction of human developmental toxicity hazard of unknown compounds with the UKN1 test system.

Publication Title

A transcriptome-based classifier to identify developmental toxicants by stem cell testing: design, validation and optimization for histone deacetylase inhibitors.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE12921
Similar gene expression profiles of sporadic, PGL2-, and SDHD-linked paragangliomas
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

The similarity in gene-expression profiles suggest that PGL2, like SDHD, is involved in the functionality of the SDH complex, and that tumor formation in these three subgroups involves the same pathways as in SDH linked paragangliomas. We were not able to clarify the identity of PGL2 on 11q13. The lack of differential gene-expression of chromosome 11 genes might indicate that chromosome 11 loss, as demonstrated in SDHD-linked paragangliomas, is an important feature in the formation of a paraganglioma regardless of the genetic background.

Publication Title

Similar gene expression profiles of sporadic, PGL2-, and SDHD-linked paragangliomas suggest a common pathway to tumorigenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE84500
TGFbeta-induced switch from adipogenic to osteogenic differentiation of human mesenchymal stem cells
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene Expression analysis of a differentiation timeseries of human Mesenchymal Stem Cells (hMSCs) in the presence of adipogenic/osteogenic factors. hMSCs differentiate into fat cells when treated with dexamethasone (10^-6 M), insulin (10 ug/ml), rosiglitazone (10^-7 M) and IBMX (250 uM). TGFbeta (5 ng/ml) inhibits this process and redirects these cells to differentiate into bone cells.

Publication Title

TGFβ-induced switch from adipogenic to osteogenic differentiation of human mesenchymal stem cells: identification of drug targets for prevention of fat cell differentiation.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon SRP150723
Effect of BMP inhibition or stimulation of primary human keratinocytes
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

BMP treatment induces expression of late differenitation genes in primary human keratinocytes. Overall design: RNA-seq analysis after treatment with EGFR inhibitor AG1478 with or without BMP27 or BMP inhibitor DMH1. each treatment and control was performed in triplicate

Publication Title

Single-Cell ID-seq Reveals Dynamic BMP Pathway Activation Upstream of the MAF/MAFB-Program in Epidermal Differentiation.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE97150
Genexpression of murine mesothelioma cell lines AC29 and AB1
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

RNA from two murine mesothelioma cell lines (AC29 and AB1) was extracted and hybridized to Affymetrix Microarrays to compare gene expression. Both mesothelioma cell lines were established following intraperitoneal introduction of crocidolite (asbestos) fibers (Davis et al. 1992) in CBA mice (AC29 cell line), and BALB/c mice (AB1).

Publication Title

Depletion of Tumor-Associated Macrophages with a CSF-1R Kinase Inhibitor Enhances Antitumor Immunity and Survival Induced by DC Immunotherapy.

Sample Metadata Fields

Sex

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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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