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accession-icon GSE23167
Expression data from DC-induced Hopx-deficient and sufficient regulatory T cells after immunization
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found that Hopx is required for the function of DC-induced regulatory T cells in vivo. We used microarrays to identify relevant Hopx-targets in such cells after antigenic re-challenge in vivo.

Publication Title

The transcription cofactor Hopx is required for regulatory T cell function in dendritic cell-mediated peripheral T cell unresponsiveness.

Sample Metadata Fields

Specimen part

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accession-icon GSE62600
Gene expression analysis of human medulloblastoma and neural stem cells
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Medulloblastoma is the most common form of malignant paediatric brain tumour and is the leading cause of childhood cancer related mortality. The four molecular subgroups of medulloblastoma that have been identified WNT, SHH, Group 3 and Group 4 - have molecular and topographical characteristics suggestive of different cells of origin. Definitive identification of the cell(s) of origin of the medulloblastoma subgroups, particularly the poorer prognosis Group 3 and Group 4 medulloblastoma, is critical to understand the pathogenesis of the disease, and ultimately for the development of more effective treatment options.

Publication Title

Gene expression analyses of the spatio-temporal relationships of human medulloblastoma subgroups during early human neurogenesis.

Sample Metadata Fields

Sex, Age

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accession-icon GSE69078
Comparison of the gene expression profiles of carfilzomib-resistant derivatives versus parental human myeloma cell lines
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

KMS-11 and KMS-34 cells were exposed to stepwise increasing concentrations of carfilzomib over a period of 18 weeks: cells adapted to growth in 4 nM carfilzomib by 4 weeks, in 6 nM in another 6 weeks and in 12 nM after a further 8 weeks. The resulting cell cultures, denoted KMS-11/Cfz and KMS-34/Cfz, respectively, retained resistance to carfilzomib even when tested after removal of selective pressure for approximately 8 weeks.

Publication Title

KLF4-SQSTM1/p62-associated prosurvival autophagy contributes to carfilzomib resistance in multiple myeloma models.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE78069
Comparative expression analysis of carfilzomib-resistant and parental LP-1 human multiple myeloma cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

LP-1 cells were exposed to stepwise increasing concentrations of carfilzomib over a period of 18 weeks: cells adapted to growth in 4 nM carfilzomib by 4 weeks, in 6 nM in another 6 weeks and in 12 nM after a further 8 weeks. The resulting cell culture, denoted LP-1/Cfz, retained resistance to carfilzomib even when tested after removal of selective pressure for approximately 8 weeks.

Publication Title

Noncanonical SQSTM1/p62-Nrf2 pathway activation mediates proteasome inhibitor resistance in multiple myeloma cells via redox, metabolic and translational reprogramming.

Sample Metadata Fields

Cell line

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accession-icon SRP062287
Research resource: global identification of estrogen receptor ß target genes in triple negative breast cancer cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The goal of this work was to identify all estrogen receptor beta target genes using RNA sequencing in MDA-MB-468 triple negative breast cancer cells engineered with inducible expression of full length estrogen receptor beta. Overall design: MDA-MB-468 breast cancer cells with inducible ERb expression (MDA-468-ERb cells) were treated in triplicate with vehicle (control, no ERb) or doxycycline (plus ERb) for 48 hr prior to treatment with 0.1% DMSO vehicle or 10 nM 17b-estradiol for 4 hr.

Publication Title

Research resource: global identification of estrogen receptor β target genes in triple negative breast cancer cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP093988
Krüppel-like Transcription Factor-10 (KLF10) Provides a Negative Feedback Mechanism to Suppress TGFß-Induced Epithelial-to-Mesenchymal Transition [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We examined transcriptome-wide effects of pertrurbation in KLF10 function (siKLF10) on TGFß-regulated genes and EMT in two different cells lines: A549 and Panc1. Overall design: We performed mRNA sequencing from A549 and Panc1 cells following following TGFß treatment and KLF10 knockdown. The mRNA-Seq includes following conditions: siControl, siKLF10, TGFß, siKLF10+TGFß (A549 and Panc1 cells). mRNA-sequencing was performed in duplicates for A549 and triplicates for Panc1 cells.

Publication Title

Krüppel-like Transcription Factor KLF10 Suppresses TGFβ-Induced Epithelial-to-Mesenchymal Transition via a Negative Feedback Mechanism.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP127668
Transcriptomic study of zinc-deficient Saccharomyces cerevisiae wild-type, atg1?, and atg41? strains
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Purpose: ATG41 is involved both in autophagy and zinc-deficient growth. The goal of this study is to compare transcriptomic profiles of wild-type and atg41? strains to discover autophagy-independent molecular phenotypes for the mutant. The atg1? mutant is a control for autophagy activity. Methods: Wild-type and mutant yeast were grown to mid-log phase in replete medium and shifted to zinc-deficient medium for 8 hours, after which, cells were harvested for RNA sequencing to detect differential gene expression. Results: Gene expression data for virtually every gene (~6,000) was obtained with ~12,000,000 reads per sample. Differential gene expression analysis showed that several hundred genes were differentially experessed in the atg41? mutant (greater than 2-fold) at an FDR of 0.5. Conclusions: Most strikingly, we found that the atg41? mutant transcriptome shows signs that sulfur metabolism is distrupted during zinc-deficinet growth. Expression of Met4 gene targets is increased. Overall design: mRNA from wild-type, atg1?, and atg41? yeast strains was prepared from zinc-deficient cultures in quadruplicate and sequenced. Single-end, 100bp sequencing was performed, using v4 SBS chemistry on an Illumina HiSeq2500 sequencer.

Publication Title

An Autophagy-Independent Role for <i>ATG41</i> in Sulfur Metabolism During Zinc Deficiency.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP076175
BRD4 localization to lineage-specific enhancers is associated with a distinct transcription factor repertoire [mRNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 21 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We examined context specific function of BRD4 in promoting lineage specific gene expression and show that BRD4 is essential for osteoblast differentiation. Overall design: We performed mRNA sequencing from hFOB cells (undifferentiated and differentiated for 5 days into osteoblastic lineage) following BRD4 inhibition by JQ1 or siRNA mediated depletion. The mRNA-Seq includes namely 7 conditions: undifferentiated hFOBs treated with DMSO or non-targeting control siRNA (siCNTR), differentiated hFOBs with DMSO or siCNTR treatments; differentiated hFOBs treated with JQ1 or two siRNAs against BRD4 (#3 & #4). The libraries were performed in triplicates.

Publication Title

BRD4 localization to lineage-specific enhancers is associated with a distinct transcription factor repertoire.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP039501
Gene expression profile of metastasis-associated neutrophils
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The goal of this experiment was to determine gene expresssion differences between neutrophils from either K14cre;CdhF/F;Trp53F/F mammary tumor-bearing mice or wild-type mice. Overall design: Neturophil expression profiles were compared between four wild-type mice and five K14cre;CdhF/F;Trp53F/F mice.

Publication Title

IL-17-producing γδ T cells and neutrophils conspire to promote breast cancer metastasis.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-MEXP-1415
Transcription profiling time series of leaves from winter wheat grown under S and N-deficient conditions
  • organism-icon Triticum aestivum
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Wheat Genome Array (wheat)

Description

Transcripomic analysis of leaf gene expression in S and N-deficient winter wheat during grain development. Tissue was harvested at anthesis and 7, 14 and 21 days post anthesis from experimental field plots.

Publication Title

Co-ordinated expression of amino acid metabolism in response to N and S deficiency during wheat grain filling.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject, Time

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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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