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accession-icon GSE64194
Expression data to investigate Costello syndrome using human iPSCs differentiated into astroglial progenitors and astrocytes
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We used microarrays to compare gene expression between three HRAS-wild type lines (13, 162d, 165d) and three HRAS-G12S mutant lines (7, 8, 16).

Publication Title

Dysregulation of astrocyte extracellular signaling in Costello syndrome.

Sample Metadata Fields

Specimen part

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accession-icon GSE55054
Astrocyte-encoded positional cues maintain sensorimotor circuit integrity
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Astrocytes, the most abundant cells in the central nervous system, promote synapse formation and help refine neural connectivity. Although they are allocated to spatially distinct regional domains during development, it is unknown whether region-restricted astrocytes are functionally heterogeneous. Here we show that postnatal spinal cord astrocytes express several region-specific genes, and that ventral astrocyte-encoded Semaphorin3a (Sema3a) is required for proper motor neuron and sensory neuron circuit organization. Loss of astrocyte-encoded Sema3a led to dysregulated motor neuron axon initial segment orientation, markedly abnormal synaptic inputs, and selective death of but not of adjacent motor neurons. Additionally, a subset of TrkA+ sensory afferents projected to ectopic ventral positions. These findings demonstrate that stable maintenance of a positional cue by developing astrocytes influences multiple aspects of sensorimotor circuit formation. More generally, they suggest that regional astrocyte heterogeneity may help to coordinate postnatal neural circuit refinement.

Publication Title

Astrocyte-encoded positional cues maintain sensorimotor circuit integrity.

Sample Metadata Fields

Specimen part

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accession-icon GSE36923
Microarray Gene Expression for Undifferentiated Mesenchymal Stem Cells, Adipogenically Differentiated and Dedifferentiation cells
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Bone marrow mesenchymal stem cells (MSC) were adipogenically differentiated followed by dedifferentiation. We are interested to know the new fat markers, adipogenic signaling pathways and dedifferentiation signaling pathways.Furthermore we are also intrested to know that how differentiated cells convert into dedifferentiated progenitor cells. To address these questions, MSC were adipogenically differentiated, followed by dedifferentiation. Finally these dedifferentiated cells were used for adipogenesis, osteogenesis and chondrogenesis. Histology, FACS, qPCR and GeneChip analyses of undifferentiated, adipogenically differentiated and dedifferentiated cells were performed. Regarding the conversion of adipogenically differentiated cells into dedifferentiated cells, gene profiling and bioinformatics demonstrated that upregulation (DHCR24, G0S2, MAP2K6, SESN3) and downregulation (DST, KAT2, MLL5, RB1, SMAD3, ZAK) of distinct genes play a curcial role in cell cycle to drive the adipogenically differentiated cells towards an arrested state to narrow down the lineage potency. However, the upregulation (CCND1, CHEK, HGF, HMGA2, SMAD3) and downregulation (CCPG1, RASSF4, RGS2) of these cell cycle genes motivates dedifferentiation of adipogenically differentiated cells to reverse the arrested state. We also found new fat markers along with signaling pathways for adipogenically differentiated and dedifferentiated cells, and also observed the influencing role of proliferation associated genes in cell cycle arrest and progression.

Publication Title

Transdifferentiation of adipogenically differentiated cells into osteogenically or chondrogenically differentiated cells: phenotype switching via dedifferentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE17105
Gene expression regulated by G-actin switch
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We analysed the G-actin regulated transcriptome by gene expression analysis using previously characterised actin binding drugs. We found many known MAL/MRTF-dependent target genes of serum response factor (SRF) as well as unknown directly regulated genes.

Publication Title

Negative regulation of the EGFR-MAPK cascade by actin-MAL-mediated Mig6/Errfi-1 induction.

Sample Metadata Fields

Time

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accession-icon GSE108595
Expression data from sorted humanized TREM2 murine microglia
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The R47H variant of TREM2 is associated with higher risk of Alzheimer's disease. We generated mice expressing the common variant or R47H variant of human TREM2

Publication Title

Humanized TREM2 mice reveal microglia-intrinsic and -extrinsic effects of R47H polymorphism.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE92693
IL-15 sustains IL-7R independent ILC2 and ILC3 development
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

ILC3 contain 3 well-defined subsets, CCR6+ ILC3, NKp46+ ILC3, and CCR6NKp46 DN ILC3. These subsets had not previously been transcriptionally compared and the extent to which they had shared or unique transcriptional profiles remained unclear.

Publication Title

IL-15 sustains IL-7R-independent ILC2 and ILC3 development.

Sample Metadata Fields

Specimen part

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accession-icon SRP180359
Epithelial mesenchymal transition (EMT) in A549 NSCLC cells. TGFbeta was used to induce EMT, RNA isolated and subjected to RNAseq on Illumina HiSeq
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The capacity of cancer cells to undergo epithelial mesenchymal trans-differentiation has been implicated as a factor driving metastasis, through the acquisition of enhanced migratory/invasive cell programs and the engagement of anti-apoptotic mechanisms promoting drug and radiation resistance. Our aim was to define molecular signaling changes associated with mesenchymal trans-differentiation in two KRas mutant NSCLC models. We focused on central transcription and epigenetic regulators predicted to be important for mesenchymal cell survival. Overall design: Haley, J.A., Haughney, E., Ullman, E., Bean, J., Haley, J.D.* and Fink, M.Y. (2014) 'Altered Transcriptional Control Networks with Trans-Differentiation of Isogenic Mutant KRas NSCLC Models' Front. Oncology, doi/10.3389/fonc.2014.00344.

Publication Title

Altered Transcriptional Control Networks with Trans-Differentiation of Isogenic Mutant-KRas NSCLC Models.

Sample Metadata Fields

Treatment, Subject

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accession-icon GSE18975
Natural variation of auxin response
  • organism-icon Arabidopsis thaliana
  • sample-icon 83 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

To assess natural variation of downstream auxin responses we subjected 7 different arabidopsis ecotypes to a time course of auxin treatments. 7d-old seedlings grown in liquid culture have been treated for 0, 30 min, 1h and 3h with 1 M IAA.

Publication Title

Natural variation of transcriptional auxin response networks in Arabidopsis thaliana.

Sample Metadata Fields

Specimen part

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accession-icon SRP151272
RNA-Seq: Smad4-iECKO vs Smad4f/f P7 isolated retinal endothelial cells (iECKO=inducible, endothelial cell specific knockout)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

To identify potential biological targets of the TGFß pathway involved in AVM formation, we performed RNA-seq on endothelial cells (ECs) isolated from a Smad4 inducible, EC specific knockout (Smad4-iECKO; Smad4f/f;Cdh5-CreERT2) mouse model that develops retinal AVMs. Overall design: We sequenced a total of 6 samples. We used three wild type samples (Smad4f/f- samples names: Lit38s45, Lit38s6, Lit40s56) and three mutant samples (Smad4f/f;Cdh5-CreERT2- sample names: Lit38s12, Lit38s37, Lit40s12). For more detailed information please see supplemental document: GSE116230_Smad4ff_vs_Smad4iECKO.report.pdf

Publication Title

Angiopoietin-2 Inhibition Rescues Arteriovenous Malformation in a Smad4 Hereditary Hemorrhagic Telangiectasia Mouse Model.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE71646
Identification of global regulators of T-helper cell lineage specification
  • organism-icon Homo sapiens
  • sample-icon 12 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

Identification of global regulators of T-helper cell lineage specification.

Sample Metadata Fields

Specimen part

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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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