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accession-icon SRP186391
Quantitative Analysis of Wild Type and Neat1 -/- Cerebral Frontal Cortex Transcriptomes
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Purpose: The goals of this study are to elucidate dowstream effects of lnc RNA, Neat1 deletion in cerebral frontal cortex of adult mice by comparing Next-generation sequencing -derived cortical transcriptome profiles (RNA-seq) between wild type and Neat1 knockout mice. Methods: Brain mRNA profiles of 2-4 moths-old wild-type (WT) and lnc RNA, Neat1 knockout (Neat1-/-) mice were generated by deep sequencing, using Illumina. Reads were mapped to mm10 reference genome using TopHat (version 2.0.9) and Bowtie (version 2.1.0), with the default parameters. Known iGenomes Ensembl mm10 were quantified by HTSeq (version 0.6.0) in intersection-strict mode. A sample-by-gene read count matrix was generated for all samples by the Ensembl genes. Scaling normalization to remove composition biases in sequencing data was applied to log(CPM) (read Counts Per Million total reads) using the trimmed mean of M-values (TMM) method. Results: RNA-seq showed near-complete depletion of Neat1 RNA levels. 1359 genes were differentially expressed in the frontal cortex of Neat1-/- mice. 25 of these differentially expressed genes withstood multiple testing corrections. Examination of RNA-seq data by principle component analysis showed two principle components that were mutually uncorrelated and orthogonal. Hierarchical cluster tree analysis showed that joined nodes from Neat1-/- samples were distanced from control subset cluster confirming the results of the PCA. Conclusions: Analyses of differentially expressed gene signature from NEAT1-/- mice revealed a significant impact on processes related to oligodendrocyte differentiation and RNA post-transcriptional modification with the underlying mechanisms involving Wnt signaling, cell contact interactions, and regulation of cholesterol/lipid metabolism. Overall design: Cerebral frontal cortex mRNA profiles of 2-4 months old wild type (WT) and Neat1 -/- mice (all females) were generated by deep sequencing (N=5 controls; N=4 Neat1 knockout).

Publication Title

The expression of long noncoding RNA NEAT1 is reduced in schizophrenia and modulates oligodendrocytes transcription.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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accession-icon SRP034832
RNAseq in IMR-32 neuroblastoma cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

IMR-32 cells were subjected to lentiviral YRNA infection or nELAVL RNAi and/or UV stress followed by RNAseq analysis to monitor RNA level changes Overall design: RNA from IMR-32 cells was Trizol extracted, Ribominus selected and submitted for high-throughput sequencing.

Publication Title

Regulatory consequences of neuronal ELAV-like protein binding to coding and non-coding RNAs in human brain.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE9770
Non-demented individuals with intermediate Alzheimer's neuropathologies - neuronal expression (6 regions)
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Layer II stellate neurons (entorhinal cortex) and layer III cortical neurons (hippocampus CA1, middle temporal gyrus, posterior cingulate, superior frontal gyrus, primary visual cortex) were gene expression profiled. Brain regions are from non-demented individuals with intermediate Alzheimer's disease neuropathologies

Publication Title

Multiscale Analysis of Independent Alzheimer's Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE84422
Molecular Signatures Underlying Selective Regional Vulnerability to Alzheimer's Disease
  • organism-icon Homo sapiens
  • sample-icon 2001 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive cognitive impairment and neurodegeneration as a result of abnormal neuronal loss. To elucidate the molecular systems associated with AD, we characterized the gene expression changes associated with multiple clinical and neuropathological traits in 1,053 postmortem brain samples across 19 brain regions from 125 persons dying with varying severities of dementia and variable AD-neuropathology severities.

Publication Title

Integrative network analysis of nineteen brain regions identifies molecular signatures and networks underlying selective regional vulnerability to Alzheimer's disease.

Sample Metadata Fields

Sex, Age, Specimen part, Race, Subject

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accession-icon SRP073495
RNA-sequencing of mouse knockout models for Cnp, Plp1, and Ugt8 in the frontal cortex and cerebellum
  • organism-icon Mus musculus
  • sample-icon 174 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Oligodendrocytes (OLs) and myelin are critical for normal brain function and they have been implicated in neurodegeneration. Human neuroimaging studies have demonstrated that alterations in axons and myelin occur early in Alzheimer's Disease (AD) course. However, the molecular mechanism underlying the role of OLs in AD remains largely unknown. In this study, we systematically interrogated OL-enriched gene networks constructed from large-scale genomic, transcriptomic, and proteomic data in human AD postmortem brain samples. These robust OL networks were highly enriched for genes associated with AD risk variants, including BIN1. We corroborated the structure of the AD OL coexpression and gene-gene interaction networks through ablation of genes identified as key drivers of the networks, including UGT8, CNP, MYRF, PLP1, NPC1, and NDGR1. Perturbations of these key drivers not only caused dysregulation in their associated network neighborhoods, but also mimicked pathways of gene expression dysregulation seen in human AD postmortem brain samples. In particular, the OL subnetwork controlled by the AD risk gene PSEN1 was strongly dysregulated in AD, suggesting a potential role of PSEN1 in disrupting the myelination pathway towards the onset of AD. In summary, this study built and systematically validated the first comprehensive molecular blueprint of OL dysregulation in AD, and identified key OL- and myelination-related genes and networks as potential candidate targets for the future development of AD therapies. Overall design: The mouse knockout models have been previously described for each of Ugt8 (Coetzee et al., 1996), Cnp (Lappe-Siefke et al., 2003), and Plp1 (Klugmann et al., 1997). For each of the two conditions studied (control and homozygous knockout mice), five mice of either sex were sacrificed at postnatal day 20 and brains were flashed-frozen until analysis. The frontal cortex (FC) and cerebellum (CBM) were dissected out and individually processed. RNA was isolated using Trizol reagent and processed using Ribo-Zero rRNA removal. RNA-sequencing was performed using the Illumina HiSeq2000 with 100 nucleotide paired-end reads. RNA-sequencing reads were mapped to the mouse genome (mm10, UCSC assembly) using Bowtie (version 2.2.3.0), TopHat (version 2.0.11), and SamTools (version 0.1.19.0) using a read length of 100. Reads were converted to counts at the gene level using HTSeq on the BAM files from TopHat2 using the UCSC known genes data set.

Publication Title

Multiscale network modeling of oligodendrocytes reveals molecular components of myelin dysregulation in Alzheimer's disease.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE53335
Regulation of inducible genes in epithelial to mesenchymal transition by chromatinized PKC-theta
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE53266
Gene expression changes in a breast cancer stem cell model.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. The epithelial cell line MCF7, can be induced to undergo EMT with the induction of PKC by PMA. 5-10% of the resulting cells have a CSC phenotype. This study looks at the transcriptome of these cells and how it differs from cells with a non-CSC phenotype.

Publication Title

Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE5122
Identification of molecular predictors of response in a study of tipifarnib treatment in relapsed and refractory AML
  • organism-icon Homo sapiens
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Gene signatures were derived to separate responders from nonresponders by tipifarnib treatment.

Publication Title

Identification of molecular predictors of response in a study of tipifarnib treatment in relapsed and refractory acute myelogenous leukemia.

Sample Metadata Fields

Sex, Age

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accession-icon SRP045890
Impact of HP1gamma and HP1gamma S83 phosphorylation on the transcriptionnal effect of PMA stimulation of mouse fibroblasts
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We have here followed the transcriptional effect of stimulation with the phorbol ester PMA in mouse fibroblasts from HP1gamma null mice recomplemented with either wild-type HP1gamma or an HP1g with an S83A mutation Overall design: Spontaneously immortalized mouse embryonic fibroblasts from HP1gamma null mice were used to stably integrate either an empty expression vector, or expression vectors for either WT or S83A mutant HP1gamma. These cells were then stimulated with PMA for 0 or 60 min. and used for transcriptome analysis by Next Generation sequencing.

Publication Title

Shigella flexneri targets the HP1γ subcode through the phosphothreonine lyase OspF.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP075283
Development and differentiation of early innate lymphoid progenitors
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Early innate lymphoid progenitors (EILP) have recently been identified in the mouse adult bone marrow as a multipotential progenitor population committed to ILC lineages, but their relationship with other described ILC progenitors is still unclear. In this study, we examine the progenitor-successor relationships between EILP, IL-7R+ common lymphoid progenitors (ALP), and ILC precursors (ILCp). Bioinformatic, phenotypical, functional, and genetic approaches collectively establish EILP as an intermediate progenitor between ALP and ILCp. Our work additionally provides new candidate regulators of ILC development and clearly defines the stage of requirement of transcription factors key for early ILC development. Overall design: transcriptional profiling of early ILC progenitors (EILP, ILCp), and common lymphoid progenitors (ALP) was performed by RNA sequencing

Publication Title

Development and differentiation of early innate lymphoid progenitors.

Sample Metadata Fields

Specimen part, Cell line, Subject

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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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