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accession-icon GSE9397
FSHD Muscle Profiles
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant disorder linked to contractions of the D4Z4 repeat array in the subtelomeric region of chromosome 4q. By comparing genome-wide gene expression data from muscle biopsies of patients with FSHD to those of 11 other neuromuscular disorders, we intend to identify disease-specific changes which are more likely to be involved in the early stages of the disease progression. The data will help to identify pathological mechanisms involved in FSHD.

Publication Title

DUX4, a candidate gene of facioscapulohumeral muscular dystrophy, encodes a transcriptional activator of PITX1.

Sample Metadata Fields

Disease, Disease stage

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accession-icon GSE3307
Comparative profiling in 13 muscle disease groups
  • organism-icon Homo sapiens
  • sample-icon 235 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Summary: Genetic disorders of muscle cause muscular dystrophy, and are some of the most common inborn errors of metabolism. Muscle also rapidly remodels in response to training and innervation. Muscle weakness and wasting is important in such conditions as aging, critical care medicine, space flight, and diabetes. Finally, muscle can also be used to investigate systemic defects, and the compensatory mechansisms invoked by cells to overcome biochemical and genetic abnormalities. Here, we provide a 13 group data set for comparative profiling of human skeletal muscle. Groups studied are: Normal human skeletal muscle, Acute quadriplegic myopathy (AQM; critical care myopathy), Juvenile dermatomyositis (JDM), Amyotophic lateral sclerosis (ALS), spastic paraplegia (SPG4; spastin), Fascioscapulohumeral muscular dystrophy (FSHD), Emery Dreifuss muscular dystrophy (both X linked recessive emerin form; autosomal dominant Lamin A/C form), Becker muscular dystrophy (partial loss of dystrophin), Duchenne muscular dystrophy (complete loss of dystrophin), Calpain 3 (LGMD2A), dysferlin (LGMD2B), FKRP (glycosylation defect; homozygous for a missense mutation). U133A and U133B microarrays are both available.

Publication Title

Nuclear envelope dystrophies show a transcriptional fingerprint suggesting disruption of Rb-MyoD pathways in muscle regeneration.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE55503
Effects of siRNA targeting PRKCD in breast cancer cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The aim was to identify genes that were commonly influenced by a siRNA targeting PRKCD in breast cancer cell lines.

Publication Title

Down Regulation of CLDND1 Induces Apoptosis in Breast Cancer Cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP078563
Unbiased genomic analysis of multiple stages of lung cancer development
  • organism-icon Mus musculus
  • sample-icon 50 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

To uncover the gene expression alterations that occur during lung cancer progression, we interrogated the gene expression state of neoplastic cells at different stages of malignant progression. We initiated tumors in KrasLSL-G12D/+;p53flox/flox;R26LSL-tdTomato (KPT) mice with a pool of barcoded lentiviral-Cre vectors and purified Tomatopositive cancer cells away from the diverse and variable stromal cell populations. Five to nine months after tumor initiation, cancer cells were isolated from individual primary tumors and metastases using fluorescence-activated cell sorting. Sequencing of the barcode region of the integrated lentiviral vectors established primary tumor-metastasis and metastasis-metastasis relationships. Tumor barcoding allowed us to unequivocally distinguish non-metastatic primary tumors (TnonMet) from those primary tumors that had seeded metastases (TMet). We profiled 10 TnonMet samples as well as TMet and metastasis (Met) samples representing 12 metastatic events. To examine additional earlier stages of lung cancer development, we also analyzed premalignant cells from hyperplasias that develop in KPT mice shortly after tumor initiation (KPT-Early; KPT-E), as well as tumors from KrasG12D;R26LSL-tdTomato (KT) mice which rarely gain metastatic ability Overall design: This study includes 52 samples: 3 KP late samples, 3KPT early samples,10 non-metastatic primary tumors, 9 metastatic primary tumors, and 27 metastasis in different organs. total RNA was isolated and prepared for sequencing using the Ovation® RNA-Seq system and Illumina TruSeq DNA kit (v2) to generate 100bp paired end reads. Reads were aligned to mm10.

Publication Title

Molecular definition of a metastatic lung cancer state reveals a targetable CD109-Janus kinase-Stat axis.

Sample Metadata Fields

Subject

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accession-icon GSE80767
Transcriptional response to mouse and human AIM2-like receptor activation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The AIM2-like Receptors Are Dispensable for the Interferon Response to Intracellular DNA.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE80766
Transcriptional response to intracellular DNA in cells lacking AIM2-like receptors
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Analysis of ALR-deficient cells indicates that ALRs are not required for the IFN response to intracellular DNA. To explore whether AIM2-like receptors activated another innate signaling pathway upon

Publication Title

The AIM2-like Receptors Are Dispensable for the Interferon Response to Intracellular DNA.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE40222
A combinatorial extracellular matrix platform identifies cell-extracellular matrix interactions that correlate with metastasis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Extracellular matrix interactions play essential roles in normal physiology and many pathological processes. Here, we report a novel screening platform capable of measuring phenotypic responses to combinations of ECM molecules. While the importance of ECM interactions in metastasis is well documented, systematic approaches to identify their roles in distinct stages of tumorigenesis have not been described. Using a genetic mouse model of lung adenocarcinoma, we measured the ECM-dependent adhesion of tumor-derived cells. Hierarchical clustering of adhesion profiles generated using this platform differentially segregated metastatic cell lines from primary tumor lines. Furthermore, we uncovered that metastatic cells selectively associate with fibronectin when in combination with galectin-3, galectin-8, or laminin. These interactions appear to be mediated in part by 31 integrin both in vitro and in vivo. We show that these galectins also correlate with human disease at both a transcriptional and histological level. Thus, our in vitro platform allowed us to interrogate the interactions of metastatic cells with their surrounding environment, and identified ECM and integrin interactions that could lead to therapeutic targets for metastasis prevention.

Publication Title

A combinatorial extracellular matrix platform identifies cell-extracellular matrix interactions that correlate with metastasis.

Sample Metadata Fields

Specimen part

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accession-icon SRP181622
REM sleep's unique associations with corticosterone regulation, apoptotic pathways and behavior in chronic stress in mice
  • organism-icon Mus musculus
  • sample-icon 308 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

One of sleep's putative functions is mediation of adaptation to waking experiences. Chronic stress is a common waking experience, however, which specific aspect of sleep is most responsive, and how sleep changes relate to behavioral disturbances and molecular correlates remain unknown. We quantified sleep, physical, endocrine, and behavioral variables, as well as the brain and blood transcriptome in mice exposed to 9 weeks of unpredictable chronic mild stress (UCMS). Comparing 46 phenotypical variables revealed that rapid-eye-movement sleep (REMS), corticosterone regulation, and coat state were most responsive to UCMS. REMS theta oscillations were enhanced, whereas delta oscillations in non-REMS were unaffected. Transcripts affected by UCMS in the prefrontal cortex, hippocampus, hypothalamus, and blood were associated with inflammatory and immune responses. A machine-learning approach controlling for unspecific UCMS effects identified transcriptomic predictor sets for REMS parameters that were enriched in 193 pathways, including some involved in stem cells, immune response, apoptosis, and survival. Only three pathways were enriched in predictor sets for non-REMS. Transcriptomic predictor sets for variation in REMS continuity and theta activity shared many pathways with corticosterone regulation, in particular pathways implicated in apoptosis and survival, including mitochondrial apoptotic machinery. Predictor sets for REMS, and anhedonia shared pathways involved in oxidative stress, cell proliferation, and apoptosis. These data identify REMS as a core and early element of the response to chronic stress, and identify apoptosis and survival pathways as a putative mechanism by which REMS may mediate the response to stressful waking experiences. Overall design: Study of transcriptomic changes in three stress- and sleep-related brain regions (prefrontal cortex, hippocampus, hypothalamus) and blood following 9 weeks of Unpredictable Chronic Mild Stress (UCMS) in mice.

Publication Title

REM sleep's unique associations with corticosterone regulation, apoptotic pathways, and behavior in chronic stress in mice.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon SRP153147
Inter-tumoral heterogeneity in SCLC is influenced by the cell-type of origin
  • organism-icon Mus musculus
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500, Illumina HiSeq 4000

Description

We describe two different routes of SCLC metastatic progression Overall design: We performed RNA-seq on primary tumors and metastasis from SCLC mouse model (Rb/p53/p130/mTmG) transduced by Ad-CMV-Cre or Ad-CGRP-Cre

Publication Title

Axon-like protrusions promote small cell lung cancer migration and metastasis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE23875
Stage-specific sensitivity to p53 restoration in lung cancer
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Stage-specific sensitivity to p53 restoration during lung cancer progression.

Sample Metadata Fields

Sex, Specimen part, Cell line

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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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