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accession-icon GSE70169
The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways
  • organism-icon Homo sapiens, Saccharomyces cerevisiae
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE22432
TGF-1 Accelerates Dendritic Cell Differentiation from Common Dendritic Cell Progenitors (CDPs) and Directs Subset Specification Towards Conventional Dendritic Cells
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Dendritic cells (DCs) in lymphoid tissue comprise conventional DCs (cDCs) and plasmacytoid DCs (pDCs) that develop from common DC progenitors (CDPs). CDPs are Flt3+c-kitintM-CSFR+ and reside in bone marrow. Here we describe a two-step culture system that recapitulates DC development from c-kithiFlt3-/lo multipotent progenitors (MPPs) into CDPs and further into cDC and pDC subsets. MPPs and CDPs are amplified in vitro with Flt3 ligand, stem cell factor, hyper-IL-6 and insulin- like growth factor-1. The four-factor cocktail readily induces self-renewal of MPPs and their progression into CDPs and has no self-renewal activity on CDPs. The amplified CDPs respond to all known DC poietins and generate all lymphoid tissue DCs in vivo and in vitro. Additionally, in vitro CDPs recapitulate the cell surface marker and gene expression profile of in vivo CDPs and possess a DC-primed transcription profile. Transforming growth factor-1 (TGF-1) impacts on CDPs and directs their differentiation towards cDCs. Genome-wide gene expression profiling of TGF-1-induced genes identified transcription factors, such as interferon regulatory factor-4 (IRF-4) and RelB, that are implicated as instructive factors for cDC subset specification. TGF-1 also induced the transcription factor inhibitor of differentiation/DNA binding 2 (Id2) that suppresses pDC development. Thus, TGF-1 directs CDP differentiation into cDC by inducing both cDC instructive factors and pDC inhibitory factors.

Publication Title

TGF-beta1 accelerates dendritic cell differentiation from common dendritic cell progenitors and directs subset specification toward conventional dendritic cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE77878
Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

T-cell Receptor Signaling Activates an ITK/NF-κB/GATA-3 axis in T-cell Lymphomas Facilitating Resistance to Chemotherapy.

Sample Metadata Fields

Specimen part, Disease stage, Cell line

View Samples
accession-icon GSE77875
Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL1; T8ML1]
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

To study differential gene expression of TCLs upon TCR signaling, three TCL primary cells and one TCL cell line T8ML1 were chosen for this study. The prmiary TCL cells consist of TCL1 and TCL2 (sezary patients) and TCL3 (PTCL, NOS patient). The TCR signaling was engaged by anti-CD3/CD28 treatment in vitro. The TCL cells were treated without/with anti-CD3/CD28 for different time periods in vitro in cell culture. The total RNA was isolated from the TCLs and subjected to affimetry microarray (GPL17692) analysis. The differential gene expression of individual TCL was identified as well as a set of common genes invloved in TCR signaling in TCLs.

Publication Title

T-cell Receptor Signaling Activates an ITK/NF-κB/GATA-3 axis in T-cell Lymphomas Facilitating Resistance to Chemotherapy.

Sample Metadata Fields

Specimen part, Disease stage, Cell line

View Samples
accession-icon GSE77876
Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL2]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

To study differential gene expression of TCLs upon TCR signaling, three TCL primary cells and one TCL cell line T8ML1 were chosen for this study. The prmiary TCL cells consist of TCL1 and TCL2 (sezary patients) and TCL3 (PTCL, NOS patient). The TCR signaling was engaged by anti-CD3/CD28 treatment in vitro. The TCL cells were treated without/with anti-CD3/CD28 for different time periods in vitro in cell culture. The total RNA was isolated from the TCLs and subjected to affimetry microarray (GPL17692) analysis. The differential gene expression of individual TCL was identified as well as a set of common genes invloved in TCR signaling in TCLs.

Publication Title

T-cell Receptor Signaling Activates an ITK/NF-κB/GATA-3 axis in T-cell Lymphomas Facilitating Resistance to Chemotherapy.

Sample Metadata Fields

Specimen part, Disease stage

View Samples
accession-icon GSE77877
Differential gene expression of T-cell lymphomas (TCL) upon engagement of T-cell receptor (TCR) signaling [TCL3]
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

To study differential gene expression of TCLs upon TCR signaling, three TCL primary cells and one TCL cell line T8ML1 were chosen for this study. The prmiary TCL cells consist of TCL1 and TCL2 (sezary patients) and TCL3 (PTCL, NOS patient). The TCR signaling was engaged by anti-CD3/CD28 treatment in vitro. The TCL cells were treated without/with anti-CD3/CD28 for different time periods in vitro in cell culture. The total RNA was isolated from the TCLs and subjected to affimetry microarray (GPL17692) analysis. The differential gene expression of individual TCL was identified as well as a set of common genes invloved in TCR signaling in TCLs.

Publication Title

T-cell Receptor Signaling Activates an ITK/NF-κB/GATA-3 axis in T-cell Lymphomas Facilitating Resistance to Chemotherapy.

Sample Metadata Fields

Specimen part, Disease stage

View Samples
accession-icon GSE68390
Comparison of Hox6 mutant and control E12.5 mouse pancreas
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Hox genes are critical developmental transcription factor. We found that in mice with disrupted expression of Hoxa6, Hoxb6 and Hoxc6 there is significantly disrupted endocrine pancreas development. We used microarray analysis to probe for possible molecular mechanisms involed in Hox6 signaling in pancreas development.

Publication Title

Mesenchymal Hox6 function is required for mouse pancreatic endocrine cell differentiation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE27702
Highly Pathogenic Avian Influenza Viruses Avoid Effective Inflammatory Response of Human Macrophages
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Macrophages were infected with low (PR8) and high pathogenic influenza viruses (FPV and H5N1). To our surprise a genome-wide comparative systems biology approach revealed that in contrast PR8 infections with HPAIV H5N1 and FPV result in a reduced immune response of human macrophages contradicting a primary role of this cell type for the cytokine storm.

Publication Title

Highly pathogenic avian influenza viruses inhibit effective immune responses of human blood-derived macrophages.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP065451
A Dual Molecular Analog Tuner for Dissecting Mammalian Protein Function
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq500

Description

Loss-of-function studies are fundamental for dissecting gene function. Yet, methods to rapidly and effectively perturb genes in mammalian cells are scarce. We present a novel system, deliverable with only two lentiviral vectors, which enables simultaneous control over two different proteins in the same cell. By harnessing the plant auxin and jasmonate hormone-induced degradation pathways, combined with RNA interference, this system allows constitutive depletion of two endogenous proteins and their replacement with two exogenous proteins whose degradation is rapidly and reversibly induced by external ligands, representing a dual analog molecular tuner. Focusing on NANOG, CHK1 and NOTCH1 in embryonic stem cells and p53 in cancer cells we have validated the efficiency, rapidity, reversibility, titratability and multiplicity of the engineered tuners, and demonstrated their potential to facilitate previously-unfeasible experimental approaches and to generate novel biological insights. Overall design: For mRNA-Seq preparation, coronatine/DMSO treated cells were collected.

Publication Title

A dual molecular analogue tuner for dissecting protein function in mammalian cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE53971
Wnt/beta-catenin-signaling in immortalized mouse adrenocortical cell line ATCL7
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

In order to investigate genes regulated by Wnt/Beta-catenin-signaling in immortalized mouse adrenocortical cells, we treated a pair of ATCL7 cell cultures, one with BIO, a small molecule mimicking Wnt/Beta-catenin-signaling, the other with a control treatment. We repeated this 3 additional times resulting in 4 pairs of samples. The Wnt/beta-catenin pathway is not basally active in ATCL7 cells, nor do these cells appear to contain any mutations in the Wnt/Beta-catenin pathway. ATCL7 cells were grown under standard conditions at 37C in a humidified incubator containing 5% CO2. 250,000 ATCL7 cells per sample were treated with 0.5uM BIO (6-Bromoindirubin-3'-oxime) or 0.01% DMSO (v/v) for 24 hours, in DMEM:F12 growth media containing 100U/mL pencillin/streptomycin, 1X insulin-transferrin-selenium-X, 0.025% fetal bovine serum and 0.025% horse serum. Cells were harvested and RNA was extracted using an RNeasy Plus Mini Kit (Qiagen). Biotinylated cDNA were prepared according to the Ambion WT kit protocol from 250 ng total RNA (GeneAtlas WT Expression Kit User Manual P/N 702935 Rev. 3). We assayed the targets with Affymetrix Mouse Gene ST 1.1 strip arrays. We modeled the data using paired T-tests for each probe-set. We also supply a supplementary file holding the data and some statistical analysis, as well as probe-set annotation that we used at that time (users may wish to obtain new annotation though). We analyzed only 28944 probe-sets with category "main", "---", and "flmrna->unmapped" according to Affymetrix annotation.

Publication Title

Wnt signaling inhibits adrenal steroidogenesis by cell-autonomous and non-cell-autonomous mechanisms.

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment

View Samples

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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