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accession-icon GSE60862
Gene-level analysis of 1231 samples originating from 134 Caucasian individuals
  • organism-icon Homo sapiens
  • sample-icon 1231 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This data set was generated by the UK Brain Expression Consortium and consists of gene expression data generated from post-mortem human brain samples, dissected from 10 brain regions and originating from a large cohort of neurologically and neuropathologically normal individuals.

Publication Title

Widespread sex differences in gene expression and splicing in the adult human brain.

Sample Metadata Fields

Sex, Disease, Subject

View Samples
accession-icon GSE60863
Exon-level analysis of 1231 samples originating from 134 Caucasian individuals
  • organism-icon Homo sapiens
  • sample-icon 1231 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This data set was generated by the UK Brain Expression Consortium and consists of gene expression data generated from post-mortem human brain samples, dissected from 10 brain regions and originating from a large cohort of neurologically and neuropathologically normal individuals.

Publication Title

Widespread sex differences in gene expression and splicing in the adult human brain.

Sample Metadata Fields

Sex, Disease, Subject

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accession-icon SRP027358
Transcriptome of Primitive Human Hematopoietic Cells: A New Resource to Find hHSC-Specific Genes
  • organism-icon Homo sapiens
  • sample-icon 134 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We analysed the transcriptome of different HSC-enriched subpopulations of cells sorted from human umbilical cord blood and isolated from several individuals with different genetic backgrounds. We aim at identifying new cell surface markers associated with human HSC and downstream mature hematopoietic cell activity. Overall design: RNA-seq of CD34+CD45RA- cord blood cells from 17 non-pooled individuals.

Publication Title

GPR56 identifies primary human acute myeloid leukemia cells with high repopulating potential in vivo.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP028567
RNA-Seq analysis of primary AML specimens exposed to AhR modulating agents
  • organism-icon Homo sapiens
  • sample-icon 121 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The goal of the study was to identify genes that are directly or indirectly coregulated by the AhR pathway in primary human AML cells. Patient AML cells were treated for 16 hours with the two indirubin derivatives 6-bromoindirubin-3''oxime (BIO), 1-Methyl-6-bromoindirubin-3''oxime (MeBIO), the AHR-antagonist SR1 (StemReginin1), combinations of BIO+SR1 and MeBIO+SR1 or DMSO alone at indicated concentrations prior to RNA extraction for sequencing. Overall design: RNA-Seq performed on 5 primary AML samples fresh (t0) and after exposure to AhR-agonists (2), -antagonist (1), and DMSO Contributor: Leucegene Project, IRIC

Publication Title

GPR56 identifies primary human acute myeloid leukemia cells with high repopulating potential in vivo.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE37060
Expression data from siSCR and siPRMT1 ES cells
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The major type of protein arginine methyltransferase is PRMT1. Since the growth of embryos from Prmt1/ mice was arrested shortly after implantation, PRMT1 must play a critical role in early mouse development.

Publication Title

PRMT1 and PRMT8 regulate retinoic acid-dependent neuronal differentiation with implications to neuropathology.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE47214
Expression data from D3, siSCR, siPRMT1 and siPRMT8 ES cell derived neurons
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

PRMT1 and PRMT8 knockdown D3 embryonic stem cells were generated (siPRMT) or as a control, scrambled sequence was introduced (siSCR).

Publication Title

PRMT1 and PRMT8 regulate retinoic acid-dependent neuronal differentiation with implications to neuropathology.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP068213
Multiplex enhancer-reporter assays uncover unsophisticated p53 enhancer logic [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Analysis of p53 binding sites using multiplex enhancer reporter assays, ChIP-seq data and RNA-seq data. Transcription factors establish and maintain the specific transcriptome of a cell by binding to genomic regulatory regions, thereby regulating the transcription of their target genes. Like many transcription factors, the DNA sequence-specific binding preferences of p53 are known. However, it remains largely unclear what distinguishes functional enhancers from other bound genomic regions that have no regulatory activity. In addition, the genome is scattered with seemingly perfect recognition sequences that remain unoccupied. To disentangle the rules of genome-wide p53 binding, we employed two complementary techniques of multiplex enhancer-reporter assays, one using barcoded reporters and the other using enhancer self-transcription. We compared the activity of more than one thousand candidate p53 enhancers under loss and gain of p53 conditions and identified several hundred high-confidence p53-responsive enhancers. Strikingly, the large majority (99%) of these target enhancers can be characterized and distinguished from negative sequences by the occurrence of a single p53 binding site. By training a machine learning classifier on these data, and integrating the resulting genome-wide predictions with fifteen publicly available human p53 ChIP-seq data sets, we identified a consensus set of 1148 functional p53 binding sites in the human genome. Unexpectedly, this direct p53 cistrome is invariably used between cell types and experimental conditions, while differences between experiments can be largely attributed to indirect non-functional binding. Our data suggest that direct p53 enhancers function in a context-independent manner and do not contain obvious combinatorial complexity of binding sites for multiple transcription factors. They represent a class of unsophisticated cell-autonomous enhancers with a single binding site, distinct from complex developmental enhancers that integrate signals from multiple transcription factors. This suggests that context-dependent regulation of p53 target genes is not encoded in the p53 enhancer, but at different upstream or downstream layers of the cell''s gene regulatory network. Overall design: RNA-seq on MCF7 cells with p53 stable knockdown.

Publication Title

Multiplex enhancer-reporter assays uncover unsophisticated TP53 enhancer logic.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP048577
BRG1 recruitment by transcription factors MITF and SOX10 defines a specific configuration of regulatory elements in the melanocyte lineage (RNA-seq)
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

Microphthalmia-associated transcription factor (MITF) is the master regulator of the melanocyte lineage. By tandem affinity purification and mass spectrometry, we present a comprehensive characterisation of the MITF interactome comprising multiple novel cofactors involved in transcription, DNA replication and repair and chromatin organisation, including a BRG1 chromatin remodelling complex comprising CHD7. BRG1 is essential for melanoma cell proliferation in vitro and for normal melanocyte development in vivo. MITF and SOX10 actively recruit BRG1 to a set of MITF-associated regulatory elements (MAREs) at active enhancers. MITF, SOX10 and YY1 bind between two BRG1-occupied nucleosomes thus defining both a combinatorial signature of transcription factors essential for the melanocyte lineage and a specific chromatin organisation of MAREs. Nevertheless, BRG1 silencing enhances MITF occupancy at MAREs showing that BRG1 acts to promote dynamic MITF interactions with chromatin. Overall design: 19 samples corresponding to mRNA profiles of 501Mel and Hermes3A after MITF, BRG1 or control shRNA-mediated knockdown were generated by deep sequencing in triplicate (in duplicate for 501_shMITF and corresponding control 501_shSCR2), using HiSeq2500.

Publication Title

Transcription factor MITF and remodeller BRG1 define chromatin organisation at regulatory elements in melanoma cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP022871
Discovery of the p53 targetome in MCF7 cells from RNA-seq data
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

RNA-seq and ChIP-seq on MCF-7 breast cancer cell line upon activation of p53 by the non-genotoxic small molecule Nutlin-3a Overall design: RNA-seq on MCF7 without (NS) or with Nutlin-3a stimulation (S), in duplicate, using illumina HiSeq 2000

Publication Title

iRegulon: from a gene list to a gene regulatory network using large motif and track collections.

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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