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accession-icon SRP093986
Next Generation Sequencing of polyA+ RNA of cultured neural stem/progenitor cells (NSC) from mouse neonatal forebrain [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

We report the application of single-molecule-based sequencing technology for high-throughput profiling of NSC transcriptome. Overall design: Wild type and Sox2-deleted NSC were sequenced; three independent samples from wild type, and three from Sox2-deleted brains (different individual mice).

Publication Title

Mapping the Global Chromatin Connectivity Network for Sox2 Function in Neural Stem Cell Maintenance.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP167706
Genome-wide analysis of astrocyte XBP1 activation and regulation of transcriptional programs in CNS cells during EAE.
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We report XBP1 activation and regulation of pro-inflammatory signaling in astrocytes, microglia, and CNS-recruited pro-inflammatory monocytes during EAE. Overall design: Analysis of RNA expression in astrocytes, microglia, and monocytes sorted by flow cytometry. Mice transduced with astrocyte-targeting lentiviruses encoding non-targeting or Xbp1-targeting shRNAs.

Publication Title

Environmental Control of Astrocyte Pathogenic Activities in CNS Inflammation.

Sample Metadata Fields

Sex, Disease, Cell line, Subject

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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

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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

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accession-icon GSE38506
Expression data from primary human mammary fibroblasts purified from disease-free women of low and high mammographic density
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Although high mammographic density (MD) is considered one of the strongest risk factors for invasive breast cancer, the genes involved in modulating this clinical feature are unknown.

Publication Title

CD36 repression activates a multicellular stromal program shared by high mammographic density and tumor tissues.

Sample Metadata Fields

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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