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accession-icon GSE10799
Gene expression profile of lung tumors
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We have investigated whether the early dissemination of tumor cells into bone marrow is associated with a specific molecular pattern in primary lung cancer

Publication Title

Genomic profiles associated with early micrometastasis in lung cancer: relevance of 4q deletion.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE43409
RORt+ Innate lymphoid cells transcriptomes after aNKp44 and cytokine stimulation
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

RORt+ innate lymphoid cells (ILC) are crucial players of innate immune responses and represent a major source of IL-22, which has an important role in mucosal homeostasis. The signals required by RORt+ ILC to express IL-22 and other cytokines, including TNF, have only partially been elucidated. Here we show that RORt+ ILC can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORt+ ILC selectively activates a coordinated pro-inflammatory program, including TNF, while cytokine stimulation induces preferentially IL-22 expression. However, combined engagement of NKp44 and cytokine receptors results in a strong synergistic effect. These data support the concept that NKp44+ RORt+ ILC can be activated without cytokines and are able to switch between IL-22 or TNF production, depending on the triggering stimulus.

Publication Title

RORγt⁺ innate lymphoid cells acquire a proinflammatory program upon engagement of the activating receptor NKp44.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP014197
tRNA fragment profiling in CLP1 mutant (kinase-dead) mice
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Loss of CLP1 activity results in the accumulation of novel sets of small RNA fragments derived from aberrant processing of tyrosine pre-tRNA. Such tRNA fragments sensitize cells to oxidative stress-induced p53 activation and p53-dependent cell death. Overall design: 2 samples, Wt and Clp1(k/k), no replicates

Publication Title

CLP1 links tRNA metabolism to progressive motor-neuron loss.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP115310
The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases VI
  • organism-icon Mus musculus
  • sample-icon 37 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Microglia play a pivotal role in the maintenance of brain homeostasis, but lose their homeostatic function during the course of neurodegenerative disorders. We identified a specific APOE-dependent molecular signature in microglia isolated from mouse models of amyotrophic lateral sclerosis, multiple sclerosis and Alzheimer’s disease (SOD1, EAE and APP-PS1) and in microglia surrounding neuritic A?-plaques in human Alzheimer’s disease brain. This is mediated by a switch from a (M0)-homeostatic to (MGnD)-neurodegenerative phenotype following phagocytosis of apoptotic neurons via the TREM2-APOE pathway. TREM2 induces APOE signaling which is a negative regulator of the transcription program in M0-homeostatic microglia. Targeting the TREM2-APOE pathway restores the M0-homeostatic signature of microglia in APP-PS1 and SOD1 mice and prevents from neuronal loss in an acute model of neurodegeneration. In SOD1 mice, TREM2 regulates MGnD in a gender-dependent manner. APOE-mediated MGnD microglia lose their tolerogenic function. Taken together, our work identifies the TREM2-APOE pathway as a major regulator of microglial functional phenotype in neurodegenerative diseases and serves as a novel target to restore homeostatic microglia. Overall design: Illumina NextSeq500 was used to identify disease-associated vs. homeostatic molecular microglia signature in microglia in different disease models and transgenic models. Bulk microglia (1,000 cells/sample) FCRLS+ sorted microglia.

Publication Title

The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP115307
The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases IV
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Microglia play a pivotal role in the maintenance of brain homeostasis, but lose their homeostatic function during the course of neurodegenerative disorders. We identified a specific APOE-dependent molecular signature in microglia isolated from mouse models of amyotrophic lateral sclerosis, multiple sclerosis and Alzheimer’s disease (SOD1, EAE and APP-PS1) and in microglia surrounding neuritic A?-plaques in human Alzheimer’s disease brain. This is mediated by a switch from a (M0)-homeostatic to (MGnD)-neurodegenerative phenotype following phagocytosis of apoptotic neurons via the TREM2-APOE pathway. TREM2 induces APOE signaling which is a negative regulator of the transcription program in M0-homeostatic microglia. Targeting the TREM2-APOE pathway restores the M0-homeostatic signature of microglia in APP-PS1 and SOD1 mice and prevents from neuronal loss in an acute model of neurodegeneration. In SOD1 mice, TREM2 regulates MGnD in a gender-dependent manner. APOE-mediated MGnD microglia lose their tolerogenic function. Taken together, our work identifies the TREM2-APOE pathway as a major regulator of microglial functional phenotype in neurodegenerative diseases and serves as a novel target to restore homeostatic microglia. Overall design: Illumina NextSeq500 was used to identify disease-associated vs. homeostatic molecular microglia signature in microglia in different disease models and transgenic models. Bulk microglia (1,000 cells/sample) FCRLS+ sorted microglia.

Publication Title

The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

View Samples
accession-icon GSE79914
Rapid and efficient generation of myelinating oligodendrocytes from human induced pluripotent stem cells using a combination of three transcription factors
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Rapid and efficient generation of oligodendrocytes from human induced pluripotent stem cells using transcription factors.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE79912
Rapid and efficient generation of myelinating oligodendrocytes from human induced pluripotent stem cells using a combination of three transcription factors [hiPSC]
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st), Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

We demonstrate that the induction of three transcription factors (SOX10, OLIG2, NKX6.2) in hiPSC-derived neural progenitor cells (hiPSC-NPC) is sufficient to rapidly generate O4+ oligodendrocytes with an efficiency of 60 to 70% within 28 days.

Publication Title

Rapid and efficient generation of oligodendrocytes from human induced pluripotent stem cells using transcription factors.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP034547
Human CLP1 mutations alter tRNA biogenesis affecting both peripheral and central nervous system function
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

We elucidate a neurological syndrome affecting both the PNS and CNS defined by CLP1 mutations that impair tRNA splicing Overall design: Identification and biochemical characterization of mutant CLP1 in human patients

Publication Title

Human CLP1 mutations alter tRNA biogenesis, affecting both peripheral and central nervous system function.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE98107
Gene expression profiling of differentiated mouse motor neurons
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

The original objectives of the study were to identify surface markers specifically expressed in motor neurons. We now use the data to profile the expression of Cdk family members in motor neurons.

Publication Title

Dual Inhibition of GSK3β and CDK5 Protects the Cytoskeleton of Neurons from Neuroinflammatory-Mediated Degeneration In Vitro and In Vivo.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP065865
Gene Networks and Blood Biomarkers of Methamphetamine-Associated Psychosis: A Preliminary Integrative RNA-Sequencing Report
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The clinical presentation, course and treatment of methamphetamine-associated psychosis (MAP) are similar to that observed in schizophrenia (SCZ) and subsequently MAP has been hypothesized as a pharmacological and environmental model of SCZ. However, several challenges currently exist in accurately diagnosing MAP at the molecular and neurocognitive level before the MAP model can contribute to the discovery of SCZ biomarkers. We directly assessed subcortical brain structural volumes and clinical parameters of MAP within the framework of an integrative genome-wide RNA-Seq blood transcriptome analysis of subjects diagnosed with MAP (N=10), METH-dependency without psychosis (MA) (N=10) and healthy controls (N=10). We used RNA-Sequencing gene expression to characterize molecular signatures associated to METH and MAP status compared to healthy control subjects. Overall design: Peripheral blood luekocytes gene expression was subject to transcriptional analysis for 10 MAP subjects, 10 subjects with METH-dependency without psychotic symptomics and 10 healthy controls.

Publication Title

Candidate gene networks and blood biomarkers of methamphetamine-associated psychosis: an integrative RNA-sequencing report.

Sample Metadata Fields

No sample metadata fields

View Samples
...

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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