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accession-icon SRP076622
Chromatin Binding of Gcn5 in Drosophila is Largely Mediated by CP190 [RNA-seq]
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

80% of the genomic binding sites of the histone acetyltransferase Gcn5 are colocalizing with CP190 binding. Depletion of CP190 reduces the number of Gcn5 binding sites and binding strength to chromatin. Binding dependency was further supported by Gcn5 mediated co-precipitation of CP190 Overall design: RNA-seq expression profiles of drosophila S2 mRNA after depletion of CP190 and Gcn5

Publication Title

Chromatin binding of Gcn5 in Drosophila is largely mediated by CP190.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE35038
DNA Damage Response and Inflammatory Signaling Limit the MLL-ENL-induced Leukemogenesis in vivo
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Activation of the MLL-ENL-ERtm oncogene initiates aberrant proliferation of myeloid progenitors. Here, we show induction of a fail-safe mechanism mediated by the DNA damage response (DDR) machinery that results in activation of the ATR/ATM-Chk1/Chk2-p53/p21 checkpoint and cellular senescence at early stages of cellular transformation caused by a regulatable MLL-ENL-ERtm in mice. Furthermore, we identified the transcription program underlying this intrinsic anti-cancer barrier, and DDR-induced inflammatory regulators that fine-tune the signaling towards senescence, thereby modulating the fate of MLL-ENL-immortalized cells in a tissue-environment-dependent manner. Our results indicate that DDR is a rate-limiting event for acquisition of stem cell-like properties in MLL-ENL-ERtm-mediated transformation, as experimental inhibition of the barrier accelerated the transition to immature cell states and acute leukemia development.

Publication Title

DNA damage response and inflammatory signaling limit the MLL-ENL-induced leukemogenesis in vivo.

Sample Metadata Fields

Specimen part, Disease stage

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accession-icon GSE103199
CTCFL
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Choice of binding sites for CTCFL compared to CTCF is driven by chromatin and by sequence preference.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE41010
Differential roles for MBD2 and MBD3 at methylated CpG islands, active promoters and exon sequences
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Differential roles for MBD2 and MBD3 at methylated CpG islands, active promoters and binding to exon sequences.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE41003
Expression data from HeLa cells after MBD2 and MBD3 knock down
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The heterogeneous collection of NuRD complexes can be grouped into the MBD2 or MBD3 containing complexes MBD2-NuRD and MBD3-NuRD. MBD2 is known to bind to methylated CpG sequences in vitro in contrast to MBD3. Although functional differences have been described, a direct comparison of MBD2 and MBD3 in respect to genome-wide binding and function has been lacking. Here we show when depleting cells for MBD2, the MBD2 bound genes increase their activity, whereas MBD2 plus MBD3 bound genes reduce their activity. Most strikingly, MBD3 is enriched at active promoters, whereas MBD2 is bound at methylated promoters and enriched at exon sequences of active genes. This suggests a functional connection between MBD2 binding to chromatin and splicing.

Publication Title

Differential roles for MBD2 and MBD3 at methylated CpG islands, active promoters and binding to exon sequences.

Sample Metadata Fields

Cell line

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accession-icon GSE52511
Comparison of gene expression in wild-type Drosophila testes with tbrd-1 mutant testes
  • organism-icon Drosophila melanogaster
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Gene expression is tightly linked to histone acetylation on lysine residues that can be recognized by bromodomains. The testis-specific bromodomain protein tBRD-1 is essential for male fertility and might act as a co-factor of testis-specifc TAFs. Here, we perform microarray analyses and demonstrate that tBRD-1 selectively controls gene expression in male germ cells

Publication Title

tBRD-1 selectively controls gene activity in the Drosophila testis and interacts with two new members of the bromodomain and extra-terminal (BET) family.

Sample Metadata Fields

Specimen part

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accession-icon SRP051170
The activation of IL-1 induced enhancers depends on TAK1 kinase activity and NF-KB p65 [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

The inflammatory gene response requires activation of the protein kinase TAK1, but it is currently unknown how TAK1-derived signals coordinate transcriptional programs in the genome. We determined the genome-wide binding of the TAK1-controlled NF-?B subunit p65 in relation to active enhancers and promoters of transcribed genes by ChIP-seq experiments. Out of 35,000 active enhancer regions, 410 H3K4me1-positive enhancers show interleukin (IL)-1-induced H3K27ac and p65 binding. Inhibition of TAK1, IKK2 or depletion of p65 blocked inducible enhancer activation and gene expression. As exemplified by the CXC chemokine cluster located on chromosome 4, the TAK1-p65 pathway also regulates the recruitment kinetics of the histone acetyltransferase CBP, of NF-?B p50 and of AP-1 transcription factors to both, promoters and enhancers. This study provides a high resolution view of epigenetic changes occurring during the IL-1 response and allows the first genome-wide identification of a novel class of inducible p65 NF-?B-dependent enhancers in epithelial cells. Overall design: RNA-seq of KB cells either untreated or treated with IL-1 alpha

Publication Title

The Activation of IL-1-Induced Enhancers Depends on TAK1 Kinase Activity and NF-κB p65.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP125977
Transcriptome analysis of PRMT6 knock-out in NT2/D1 cells
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

Whole transcriptome for PRMT6 knock-out and control NT2/D1 cells with and without ATRA (all-trans retinoic acid) was sequenced. These samples were compared to each other to find differentially regulated genes and PRMT6-dependent transcriptome in pluripotency and differentiating cells. Overall design: Examining of PRMT6-dependent transcriptome in NT2/D1 cells using RNAseq.

Publication Title

Genomic Location of PRMT6-Dependent H3R2 Methylation Is Linked to the Transcriptional Outcome of Associated Genes.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP096557
Widespread Influence of 3'-end Structures on Mammalian mRNA Processing and Stability [CENPB-3''-end-library]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Understanding the physiological relevance of structures in mammalian mRNAs remains elusive, especially considering the global unfolding of mRNA structures in eukaryotic organisms recently examined, as well as the decade-long observation that mRNAs generally seem no more likely than random sequences to be stably folded. Here we show that RNA secondary structures, mostly weak and close-to-random, facilitate the 3'-end processing of thousands of human mRNAs by juxtaposing poly(A) signals (PASs) and cleavage sites that are otherwise too far apart. Folding of these 3'-end structures also enhances mRNA stability. Global structure probing shows that 3'-end regions are indeed folded in cells despite substantial unfolding of PAS-upstream regions. Analyses of thousands of ectopically expressed variants prove that folding both enhances processing and increases stability. Mutagenesis of a genomic locus further implicates structure-controlled processing in regulating neighboring gene expression. These results reveal widespread roles for RNA structure in mammalian mRNA biogenesis and metabolism. Overall design: This series includes 8 samples designed to measure the efficiency of 3'' end processing from a reporter library expressed in HEK293T cells and HeLa cells, in steady state or in nascent RNAs (by 4sU labeling and capture).

Publication Title

Widespread Influence of 3'-End Structures on Mammalian mRNA Processing and Stability.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP012265
Small-RNAs in L4 and young adult stages
  • organism-icon Caenorhabditis elegans
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

Small endogenous C. elegans RNAs from L4 and young adult worms were prepared for sequencing using a protocol derived from Batista et al., (2008) and Lau et al. (2001). The small-RNA libraries were constructed using a method that does not require a 5' monophosphate (called 5' monophosphate-independent method, Ambros et al., 2003) to profile secondary siRNAs that have 5' triphosphorylated G. All preprocessed small-RNA reads were mapped to genome (ce6), allowing no mismatches. After excluding miRNAs, 21U RNAs, rRNAs, and other structural ncRNAs, the remaining reads were classified as 22G RNAs, 26G RNAs, and other siRNAs, based on their length and 5' terminal nucleotide. Overall design: Small-RNA libraries were sequenced in L4 and young adult stages in C.elegans.

Publication Title

Long noncoding RNAs in C. elegans.

Sample Metadata Fields

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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