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accession-icon GSE103902
Master retinal transcription factors define a subgroup-specific photoreceptor program and implicate novel dependencies in medulloblastoma
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

We used microarrays to compare gene expression between shRNA targeting NRL and control replicates in D458Med cell line.

Publication Title

NRL and CRX Define Photoreceptor Identity and Reveal Subgroup-Specific Dependencies in Medulloblastoma.

Sample Metadata Fields

Cell line

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accession-icon SRP061329
The LIN28B/let-7 axis is a novel therapeutic pathway in Multiple Myeloma
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

MYC is a major oncogenic driver of Multiple Myeloma (MM) and yet almost no therapeutic agents exist that target MYC in MM. Here we report that the let-7 biogenesis inhibitor LIN28B correlates with MYC expression in MM and is associated with adverse outcome. We also demonstrate that the LIN28B/let-7 axis modulates the expression of MYC, itself a let-7 target. Further, perturbation of the axis regulates the proliferation of MM cells in vivo in a xenograft tumor model. RNA sequencing and gene set enrichment analyses of CRISPR-engineered cells further suggest that the LIN28/let-7 axis regulates MYC and cell cycle pathways in MM. We provide proof-of-principle for therapeutic regulation of MYC through let-7 with an LNA-GapmeR containing a let-7b mimic in vivo, demonstrating that high levels of let-7 expression repress tumor growth by regulating MYC expression. These findings reveal a novel mechanism of therapeutic targeting of MYC through the LIN28B/let-7 axis in MM that may impact other MYC dependent cancers as well. Overall design: RNA sequencing of MOLP-8 cells transduced with lentiCRISPRv2 scrambled control or containing a sgRNA against LIN28B. Both control and LIN28B KO cells were sequenced in triplicate.

Publication Title

The LIN28B/let-7 axis is a novel therapeutic pathway in multiple myeloma.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP117267
A map of gene expression in neutrophil-like cell lines
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report gene expression data for the human cell lines HL-60 and PLB-985, which serve as models for human neutrophils. We measured gene expression using RNA-Seq for these cell lines both prior and after differentiation into a neutrophil-like state using two differentiation protocols (treatment with DMSO or treatment with DMSO and replacement of serum with Nutridoma). Overall design: HL-60 and PLB-985 cells grown in culture were processed for RNA-Seq both before and after differentiation for six days in media supplemented with 1.3% dimethyl sulfoxide (DMSO). The cell lines were also analyzed after differentiation for six days in media with 1.3% DMSO, reduced serum (0.5% FBS), and Nutridoma-CS (2%). PLB-985 cells were also analyzed at intermediate time points of 2 days and 4 days with the Nutridoma protocol.

Publication Title

A map of gene expression in neutrophil-like cell lines.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE14402
TNF-a-induced MEK/ERK-dependent regulation of Cartilage Matrix Genes
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

TNF-a is increased in the synovial fluid of patients with rheumatoid arthritis and osteoarthritis. TNF-a activates MEK/ERK in chondrocytes; however the overall functional relevance of MEK/ERK to TNF-a-regulated gene expression in chondrocytes is unknown. Chondrocytes were treated with TNF-a with or without the MEK1/2 inhibitor U0126 for 24 h. Microarray analysis was used to identify genes regulated by TNF-a in a MEK1/2-dependent fashion.

Publication Title

Egr-1 inhibits the expression of extracellular matrix genes in chondrocytes by TNFalpha-induced MEK/ERK signalling.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE18623
E. coli gene expression following CHIR-090 treatment
  • organism-icon Escherichia coli
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

CHIR-090 is an inhibitor of lipid A biosytnesis. CHIR-090 treatment on E. coli sinificantly increased the expression of fatty acid biosythesis gene fabA and fabB.

Publication Title

Transcriptional regulation of membrane lipid homeostasis in Escherichia coli.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29344
Analysis of gene co-expression networks in skin cells exposed to different doses of ionising radiation at different time points
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Most studies have analysed the effects of high dose radiation such as atomic bomb survivors in Japan, people exposed during the Chernobyl nuclear accident, patients undergoing radiation therapy, uranium miners, etc. However, it has been difficult to measure and assess the risk of cancer in people exposed to lower doses of ionising radiation, such as the people living at high altitudes, who are exposed to more natural background radiation from cosmic rays than people at sea level. We measured the genomic response to X-ray ionising radiation (10 cGy and 100 cGy) in a skin tissue model to compare the effects of low and high dose ionising radiation at different time points. The microarray data was then analysed using state-of-the art upside-down pyramid computational systems biology methods to identify genes contributing to the difference in the response to the different radiation doses.

Publication Title

Comparison of low and high dose ionising radiation using topological analysis of gene coexpression networks.

Sample Metadata Fields

Time

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accession-icon GSE8590
Overview of gene expression alternatively modulated during the differentiation of human embryonic stem cells (hES)
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The transcriptome analysis was performed in triplicate using two human embryonic stem cells lines (hES_VUB01 and hES_SA01) by comparing the expression profiles of the undifferentiated hES cells and two types of progenitors derived from the hES cell lines: Neural progenitors (NPC) and Mesodermal progenitors (MSC).

Publication Title

Global transcriptional profiling of neural and mesenchymal progenitors derived from human embryonic stem cells reveals alternative developmental signaling pathways.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7598
Identification and characterization of genes expressed in the mouse ZPA using a novel microarray approach
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Comparing gene expression of cells from the E10.5 limb bud ZPA and the rest of the E10.5 limb bud from Shhgfpcre heterozygotes separated by FACS.

Publication Title

Identification of genes expressed in the mouse limb using a novel ZPA microarray approach.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP051737
Functional characterization of human T cell hyporesponsiveness induced by CTLA4-Ig
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

During activation, T cells integrate multiple signals from APCs and cytokine milieu. The blockade of these signals can have clinical benefits as exemplified by CTLA4-Ig, which blocks interaction of B7 co-stimulatory molecules on APCs with CD28 on T cells. Variants of CTLA4-Ig, abatacept and belatacept are FDA approved as immunosuppressive agents in arthritis and transplantation whereas murine studies suggested that CTLA4-Ig can be beneficial in a number of other diseases. However, detailed analysis of human CD4 cell hyporesponsivness induced by CTLA4-Ig has not been performed. Herein, we established a model to study effect of CTLA4-Ig on the activation of human naïve T cells in a human mixed lymphocytes system. Comparison of human CD4 cells activated in the presence or absence of CTLA4-Ig, showed that co-stimulation blockade during TCR activation does not affect NFAT signaling but results in decreased activation of NF-kB and AP-1 transcription factors followed by profound decrease in proliferation and cytokine production. The resulting T cells become hyporesponsive to secondary activation and, although capable of receiving TCR signals, fail to proliferate or produce cytokines, demonstrating properties of anergic cells. However, unlike some models of T cell anergy, these cells did not possess increased levels of TCR signaling inhibitor CBLB. Rather, the CTLA4-Ig induced hyporesponsiveness was associated with an elevated level of p27kip1 cyclin-dependent kinase inhibitor. Overall design: Time series. Human resting and activated T cell dUTP mRNA-Seq profiles were generated on Illumina HiSeq2500

Publication Title

Functional characterization of human T cell hyporesponsiveness induced by CTLA4-Ig.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE68745
Expression data from wildtype and Tfr1 heart KO mice
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We deleted Tfr1 in the heart to determine the role of Tfr1 in iron uptake in normal cardiac funciton We used microarrays to identify global gene changes associated with deletion of Tfr1 in skeletal muscle

Publication Title

Lethal Cardiomyopathy in Mice Lacking Transferrin Receptor in the Heart.

Sample Metadata Fields

Age, 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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