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accession-icon GSE57417
Role of Blimp-1 in programing Th effector cells into IL-10 producers
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Gene expression profiling on IL-10-secreting and non-secreting murine Th1 cells, stimulated in the presence or absence of the Notch ligand Delta-like 4 (Dll4), was performed to identify transcription factors co-expressed with IL-10.

Publication Title

Role of Blimp-1 in programing Th effector cells into IL-10 producers.

Sample Metadata Fields

Specimen part

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accession-icon GSE103348
A mouse model for embryonal tumors with multilayered rosettes uncovers the therapeutic potential of Sonic-hedgehog inhibitors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Embryonal Tumors with Multilayered Rosettes (ETMRs) have recently been described as a new entity of rare pediatric brain tumors with fatal outcome. We show here that ETMRs are characterized by a parallel activation of Shh- and Wnt-signaling. Co-activation of these pathways in murine neural precursors is sufficient to induce ETMR-like tumors in vivo that resemble their human counterparts based on histology and global gene expression analyses, and point to apical radial glia cells as the possible tumor cell-of-origin. Overexpression of LIN28A, which is a hallmark of human ETMRs, augments Sonic Hedgehog (Shh)- and Wnt-signaling in these precursor cells through downregulation of let7-miRNA, and LIN28A/let7a interaction with the Shh-pathway was detected at the level of Gli mRNA. Finally, human ETMR cells that were transplanted into immunocompromised host mice were responsive to the Shh-inhibitor Arsenic trioxide (ATO). Our findings provide a novel mouse model to study this tumor type, demonstrate the driving role of Wnt- and Shh-activation in the growth of ETMRs and propose downstream inhibition of Shh-signaling as a therapeutic option for patients with ETMRs.

Publication Title

A mouse model for embryonal tumors with multilayered rosettes uncovers the therapeutic potential of Sonic-hedgehog inhibitors.

Sample Metadata Fields

Specimen part

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accession-icon GSE63561
Prenatal alcohol exposure alters steady-state and activated gene expression in the adult rat brain
  • organism-icon Rattus norvegicus
  • sample-icon 192 Downloadable Samples
  • Technology Badge IconIllumina ratRef-12 v1.0 expression beadchip

Description

Background: Prenatal alcohol exposure (PAE) is associated with alterations in numerous physiological systems, including the stress and immune systems. We have previously shown that PAE increases the course and severity of arthritis in an adjuvant-induced arthritis (AA) model. While the molecular mechanisms underlying these effects are not fully known, changes in neural gene expression are emerging as important factors in the etiology of PAE effects. As the prefrontal cortex (PFC) and hippocampus (HPC) play key roles in neuroimmune function, PAE-induced alterations to their transcriptome may underlie abnormal steady-state functions and responses to immune challenge. The current study examined brains from adult PAE and control females from our recent AA study to determine whether PAE causes long-term alterations in gene expression and whether these mediate the altered severity and course of arthritis in PAE females Methods: Adult females from PAE, pair-fed [PF], and ad libitum-fed control [C]) groups were injected with either saline or complete Freunds adjuvant. Animals were terminated at the peak of inflammation or during resolution (days 16 and 39 post-injection, respectively); cohorts of saline-injected PAE, PF and C females were terminated in parallel. Gene expression was analyzed in the PFC and HPC using whole genome mRNA expression microarrays. Results: Significant changes in gene expression in both the PFC and HPC were found in PAE compared to controls in response to ethanol exposure alone (saline-injected females), including genes involved in neurodevelopment, apoptosis, and energy metabolism. Moreover, in response to inflammation (adjuvant-injected females), PAE animals showed unique expression patterns, while failing to exhibit the activation of genes and regulators involved in the immune response observed in control and pair-fed animals. Conclusions: These results support the hypothesis that PAE affects neuroimmune function at the level of gene expression, demonstrating long-term effects of PAE on the CNS response under steady-state conditions and following an inflammatory insult. Key words: prenatal alcohol exposure (PAE), ethanol, inflammation, arthritis, gene expression, rat.

Publication Title

Prenatal alcohol exposure alters steady-state and activated gene expression in the adult rat brain.

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon SRP059955
Characterization of pro- and anti-inflammatory activation states in embryonic stem cell derived microglia
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HiScanSQ

Description

Embryonic stem cell derived microglia (ESdM) were treated with different inflammatory stimulants to analyze their ability to adopt different activation states. These were characterized using ELISA, flow cytometry, quantitative real time PCR, and RNA-sequencing. Overall design: Analysis of cytokine secretion, cell surface marker, gene expression, and RNA-seq expression data of differentially activated ESdM

Publication Title

Characterization of inflammatory markers and transcriptome profiles of differentially activated embryonic stem cell-derived microglia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE36575
Effect of NPAP1/C15orf2 overexpression on transcriptome of HEK293 cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To gain insight into the function of Nuclear pore associated protein 1 (NPAP1, formerly C15orf2), we overexpressed NPAP1 in HEK293 cells. We detected no significant difference between NPAP1-expression of induced and uninduced cells in three technical replicates, exept for an approximately 10-fold increase in the NPAP1 transcript itself. This indicates that overexpression of NPAP1 does not change mRNA expression profiles of HEK293 cells. We used microarrays to investigate global gene expression changes depending on the level of NPAP1/C15orf2

Publication Title

The imprinted NPAP1/C15orf2 gene in the Prader-Willi syndrome region encodes a nuclear pore complex associated protein.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE81666
Expression data of nuclear mRNA export mutant rae1-167 cells
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

rae1 is an essential gene and encodes one of nuclear pore complex. rae1-167 mutant cells show rapid accumulation of polyA-RNA in the nucleus at 36C followed by protein accumulation, suggesting that accumulated nuclear mRNA influences nucelar cytooplasmic transport.

Publication Title

A systematic genomic screen implicates nucleocytoplasmic transport and membrane growth in nuclear size control.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE30873
Effects of caspase-8 deletion in the intestinal epithelium
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Caspase-8 is a cystein protease involved in regulating apoptosis. The function of caspase-8 was studied in the intestinal epithelium, using mice with an intestinal epithelial cell specific deletion of caspase-8.

Publication Title

Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE12211
Gene expression of CML CD34+ cells during Imatinib therapy
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Imatinib has become the current standard therapy for patients with chronic myelogenous leukaemia (CML). For a better understanding of the Imatinib-related molecular effects in vivo, we assessed gene expression profiles of Philadelphia Chromosome positive (Ph+) CD34+ cells from peripheral blood of 6 patients with de novo CML in chronic phase. After 7 days of treatment with Imatinib the Ph+ CD34+ cells were reassessed to look for changes in the transcriptome. The expression level of 303 genes was significantly different comparing the transcriptome of the Ph+ CD34+ cells before and after 7 days of Imatinib therapy (183 down-regulated, 120 up-regulated, lower bound 1.2-fold). For a substantial number of genes governing cell cycle and DNA replication, the level of expression significantly decreased (CDC2, RRM2, PCNA, MCM4). On the other hand, therapy with Imatinib was associated with an increase of genes related to adhesive interactions, such as L-selectin or CD44. A group of 8 genes with differential expression levels were confirmed using a gene specific quantitative real-time PCR. Thus, during the first week of treatment, Imatinib is preferentially counteracting the bcr-abl induced effects related to a disturbed cell cycle and defective adhesion of leukemic Ph+ CD34+ cells.

Publication Title

Early in vivo changes of the transcriptome in Philadelphia chromosome-positive CD34+ cells from patients with chronic myelogenous leukaemia following imatinib therapy.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP109169
Thiol-linked alkylation for the metabolic sequencing of RNA [SLAM-seq pulse/chase labeling in wildtype mES cells]
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gene expression profiling by high-throughput sequencing reveals qualitative and quantitative changes in RNA species at steady-state but obscures the intracellular dynamics of RNA transcription, processing and decay. We developed thiol(SH)-linked alkylation for the metabolic sequencing of RNA (SLAM-seq), an orthogonal chemistry-based epitranscriptomics-sequencing technology that uncovers 4-thiouridine (s4U)-incorporation in RNA species at single-nucleotide resolution. In combination with well-established metabolic RNA labeling protocols and coupled to standard, low-input, high-throughput RNA sequencing methods, SLAM-seq enables rapid access to RNA polymerase II-dependent gene expression dynamics in the context of total RNA. When applied to mouse embryonic stem cells, SLAM-seq provides global and transcript-specific insights into pluripotency-associated gene expression. We validated the method by showing that the RNA-polymerase II-dependent transcriptional output scales with Oct4/Sox2/Nanog-defined enhancer activity; and provides quantitative and mechanistic evidence for transcript-specific RNA turnover mediated by post-transcriptional gene regulatory pathways initiated by microRNAs and N6-methyladenosine. SLAM-seq facilitates the dissection of fundamental mechanisms that control gene expression in an accessible, cost-effective, and scalable manner. Overall design: Wildtype mouse embryonic stem cells (mES cells) were subjected to s4U metabolic RNA labeling for 24 h (pulse, 100 µM s4U), followed by washout (chase) using non-thiol-containing uridine. Total RNA was prepared at various time points along the chase (0h, 0.5h, 1h, 3h, 6h, 12h, and 24h). Total RNA was then subjected to alkylation and mRNA 3' end sequencing library preparation (QuantSeq, Lexogen).

Publication Title

Quantification of experimentally induced nucleotide conversions in high-throughput sequencing datasets.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
accession-icon SRP109094
Thiol-linked alkylation for the metabolic sequencing of RNA [Transcriptional inhibition by Actinomycin D]
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Gene expression profiling by high-throughput sequencing reveals qualitative and quantitative changes in RNA species at steady-state but obscures the intracellular dynamics of RNA transcription, processing and decay. We developed thiol(SH)-linked alkylation for the metabolic sequencing of RNA (SLAM-seq), an orthogonal chemistry-based epitranscriptomics-sequencing technology that uncovers 4-thiouridine (s4U)-incorporation in RNA species at single-nucleotide resolution. In combination with well-established metabolic RNA labeling protocols and coupled to standard, low-input, high-throughput RNA sequencing methods, SLAM-seq enables rapid access to RNA polymerase II-dependent gene expression dynamics in the context of total RNA. When applied to mouse embryonic stem cells, SLAM-seq provides global and transcript-specific insights into pluripotency-associated gene expression. We validated the method by showing that the RNA-polymerase II-dependent transcriptional output scales with Oct4/Sox2/Nanog-defined enhancer activity; and provides quantitative and mechanistic evidence for transcript-specific RNA turnover mediated by post-transcriptional gene regulatory pathways initiated by microRNAs and N6-methyladenosine. SLAM-seq facilitates the dissection of fundamental mechanisms that control gene expression in an accessible, cost-effective, and scalable manner. Overall design: 5 µg/ml Actinomycin D was added to wildtype mouse embryonic stem (mES) cells and total RNA was prepared at various time points after addition of Actinomycin D (0h, 0.25h, 0.5h, 1h, 3h and 10h). Total RNA was subjected to mRNA 3' end library preparation (QuantSeq, Lexogen) and high througput sequencing.

Publication Title

Quantification of experimentally induced nucleotide conversions in high-throughput sequencing datasets.

Sample Metadata Fields

Specimen part, Treatment, Subject

View Samples
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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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