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accession-icon GSE76283
Expression data of Normal versus Mutant MPS VII Bl6 mouse
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We used microarray to detect pathway differences in the hippocampus in mucopolysaccharidosis type VII ( MPS VII ), a mouse model of a lysosomal storage disease

Publication Title

Integrated analysis of proteome and transcriptome changes in the mucopolysaccharidosis type VII mouse hippocampus.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE70025
Oncogenic CARMA1 couples NF-B and -Catenin signaling in diffuse large B cell lymphomas
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Constitutive activation of the anti-apoptotic NF-B signaling pathway is a hallmark of the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphomas (DLBCL) that is characterized by adverse survival. Recurrent oncogenic mutations are found in the scaffold protein CARMA1 (CARD11) that connects B-cell receptor (BCR) signaling to the canonical NF-B pathway. We asked how far additional downstream processes are activated and contribute to the oncogenic potential of DLBCL-derived CARMA1 mutants. To this end, we expressed oncogenic CARMA1 mutants in the NF-B negative DLBCL lymphoma cell line BJAB. By a proteomic approach we identified recruitment of -Catenin and its destruction complex consisting of APC, AXIN1, CK1 and GSK3 to oncogenic CARMA1. Recruitment of the -Catenin destruction complex was independent of CARMA1-BCL10-MALT1 (CBM) complex formation or constitutive NF-B activation and promoted the stabilization of -Catenin. Elevated -Catenin expression was detected in cell lines and biopsies from ABC DLBCL that rely on chronic BCR signaling. Increased -Catenin amounts alone were not sufficient to induce classical WNT target gene signatures, but could augment TCF/LEF dependent transcriptional activation in response to WNT signaling. In conjunction with NF-B, -Catenin enhanced expression of immune suppressive IL-10 and repressed anti-tumoral CCL3, indicating that -Catenin may induce a favorable tumor microenvironment. Thus, parallel activation of NF-B and -Catenin signaling by gain-of-function mutations in CARMA1 can augment WNT stimulation and is required for maintaining high expression of distinct NF-B target genes and can thereby trigger cell intrinsic and extrinsic processes that promote DLBCL lymphomagenesis.

Publication Title

Oncogenic CARMA1 couples NF-κB and β-catenin signaling in diffuse large B-cell lymphomas.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE26051
Analysis of Human Tendinopathy Gene Expression
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Chronic tendon injuries, also known as tendinopathy, are common among professional and recreational athletes. These injuries result in a significant amount of morbidity and health care expenditure and yet little is known about the molecular mechanism leading to tendinopathy. We have used histological evaluation and molecular profiling to determine the gene expression changes in 23 human patients undergoing surgical procedures for the treatment of chronic tendinopathy. Diseased tendons have altered extracellular matrix, fiber disorientation, increased cellular content and vasculature and the absence of inflammatory cells. Global gene expression profiling identified 1783 transcripts with significant different expression patterns in the diseased tendons. Global pathway analysis further suggests altered expression of extracellular matrix proteins and the lack of an appreciable inflammatory response. We have identified pathways and genes regulated in tendinopathy samples that will help contribute to the understanding of the disease towards the development of novel therapeutics.

Publication Title

Regulation of gene expression in human tendinopathy.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Subject

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accession-icon GSE25908
Distinct Protein Degradation Induced by Different Disuse Models of Skeletal Muscle Atrophy
  • organism-icon Mus musculus
  • sample-icon 111 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Skeletal muscle atrophy is a consequence of many diseases, environmental insults, inactivity, age and injury. Atrophy is characterized by active degradation and removal of contractile proteins and a reduction in fiber size. Animal models have been extensively used to identify pathways leading to atrophic conditions. Here we have used genome-wide expression profiling analysis and quantitative PCR to identify the molecular changes that occur in two clinically relevant animal mouse models of muscle atrophy, hindlimb casting and Achilles tendon laceration (tenotomy). Gastrocnemius muscle samples were collected 2, 7 and 14 days after insult. The total amount of muscle loss as measured by wet weight and muscle fiber size was equivalent between models, although tenotomy resulted in a more rapid induction of muscle atrophy. Furthermore, tentomy resulted in the regulation of significantly more mRNA transcripts then casting. Analysis of the regulated genes and pathways suggest that the mechanism of atrophy is distinct between these models. The degradation following casting appears ubiquitin-proteasome-mediated while degradation following tenotomy appears lysosomal and matrix-metalloproteinase (MMP)-mediated. This data suggests that there are multiple mechanisms leading to muscle atrophy and that specific therapeutic agents may be necessary to combat the atrophy seen under different conditions.

Publication Title

Distinct protein degradation profiles are induced by different disuse models of skeletal muscle atrophy.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon GSE76148
Genome wide comparison of the inducible transcriptomes of CAR, PXR and PPAR in primary human hepatocytes
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To identify the CAR-, PXR- and PPAR-specific genome-wide expression changes, hepatocyte cultures from six individual donors were treated with the prototypical ligands for

Publication Title

Genomewide comparison of the inducible transcriptomes of nuclear receptors CAR, PXR and PPARα in primary human hepatocytes.

Sample Metadata Fields

Sex, Age

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accession-icon SRP075699
Identification of a distinct IL-10 producing subset of innate lymphoid type-2 effector cells with regulatory potential
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconNextSeq 500, Ion Torrent Proton

Description

ILC210 represent a distinct effector population of ILC2 cells that have regulatory potential Overall design: comparison between ILC2 cells with IL-33 stimulation or not on transcriptome change

Publication Title

Alternative activation generates IL-10 producing type 2 innate lymphoid cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP054249
Innate lymphoid cell development requires TOX-dependent generation of a common ILC progenitor
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Subtypes of innate lymphoid cells (ILC), defined by effector function and transcription factor expression, have recently been identified. In the adult, ILC derive from common lymphoid progenitors in bone marrow, although transcriptional regulation of the developmental pathways involved remains poorly defined. TOX is required for development of lymphoid tissue inducer cells, a type of ILC3 required for lymph node organogenesis, and NK cells, a type of ILC1. We show here that production of multiple ILC lineages requires TOX, as a result of TOX-dependent development of common ILC progenitors. Comparative transcriptome analysis demonstrated failure to induce various aspects of the ILC gene program in the absence of TOX, implicating this nuclear factor as a key early determinant of ILC lineage specification. Overall design: TOX KO vs. wild tyype

Publication Title

The development of innate lymphoid cells requires TOX-dependent generation of a common innate lymphoid cell progenitor.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE90954
Effect of TGFb treatment (1 ng/ml) on gene expression in Hepa1-6 cells
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The goal of the study is a high-throughput evaluation of the effect of TGFb treatment on gene expression.

Publication Title

Resolving the Combinatorial Complexity of Smad Protein Complex Formation and Its Link to Gene Expression.

Sample Metadata Fields

Specimen part

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accession-icon GSE145935
Transcriptomic analysis of human astrocytes in vitro reveals hypoxia-induced mitochondrial dysfunction, modulation of metabolism and dysregulation of the immune response
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Changes in the transcriptomic profile of the Sciencell human astrocytes, after hypoxia treatment were compared to control cells receiving no treatment, to identify differentially expressed genes and pathways.

Publication Title

Transcriptomic Analysis of Human Astrocytes In Vitro Reveals Hypoxia-Induced Mitochondrial Dysfunction, Modulation of Metabolism, and Dysregulation of the Immune Response.

Sample Metadata Fields

Specimen part

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accession-icon GSE102937
Mechanistic differences in neuropathic pain modalities revealed by correlating behavior with global expression profiling
  • organism-icon Mus musculus
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Mechanistic Differences in Neuropathic Pain Modalities Revealed by Correlating Behavior with Global Expression Profiling.

Sample Metadata Fields

Sex, Specimen part, Treatment

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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