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accession-icon SRP170747
Deciphering the 'm6A code' via quantitative profiling of m6A at single-nucleotide resolution [II]
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

N6-methyladenosine (m6A) is the most abundant modification on mRNA, and is implicated in critical roles in development, physiology and disease. A major challenge in the field has been the inability to quantify m6A stoichiometry and the lack of antibody-independent methodologies for interrogating m6A. Here, we develop MASTER-seq for systematic quantitative profiling of m6A at single nucleotide resolution, building on differential cleavage by an RNAse at methylated sites. MASTER-seq permitted validation and de novo discovery of m6A sites, calibration of the performance of antibody based approaches, and quantitative tracking of m6A dynamics in yeast gametogenesis and mammalian differentiation. We discover that m6A stoichiometry is 'hard-coded' in cis via a simple and predictable code. This code accounts for ~50% of the variability in methylation levels and allows accurate prediction of m6A loss/acquisition events across evolution. MASTER-seq will allow quantitative investigation of m6A regulation in diverse cell types and disease states. Overall design: 10 samples were analyzed: EBS WT and Metll3 -/- with two replicates each and ESC WT and Mettld -/- with three replicates

Publication Title

Deciphering the "m<sup>6</sup>A Code" via Antibody-Independent Quantitative Profiling.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP170748
De novo detection of m6A modification in Saccharomyces cerevisiae at single nucleotide resolution
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

N6-methyladenosine (m6A) is the most abundant modification on mRNA, and is implicated in critical roles in development, physiology and disease. A major challenge in the field has been the inability to quantify m6A stoichiometry and the lack of antibody-independent methodologies for interrogating m6A. Here, we develop MASTER-seq for systematic quantitative profiling of m6A at single nucleotide resolution, building on differential cleavage by an RNAse at methylated sites. MASTER-seq permitted validation and de novo discovery of m6A sites, calibration of the performance of antibody based approaches, and quantitative tracking of m6A dynamics in yeast gametogenesis and mammalian differentiation. We discover that m6A stoichiometry is 'hard-coded' in cis via a simple and predictable code. This code accounts for ~50% of the variability in methylation levels and allows accurate prediction of m6A loss/acquisition events across evolution. MASTER-seq will allow quantitative investigation of m6A regulation in diverse cell types and disease states. Overall design: 8 samples are analyzed: IP and background for IME4 mutant and WT with 2 biological replicates for each condition

Publication Title

Deciphering the "m<sup>6</sup>A Code" via Antibody-Independent Quantitative Profiling.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE27222
Gene expression data for the budding yeast mutants pol30-8, dot1 and pol30-8 dot1
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The mutation in the budding yeast gene PCNA, pol30-8, as well as deletion of DOT1 (dot1), encoding the only histone H3 K79 methyltransferase in budding yeast, have been implicated in telomeric silencing. To further analyze these mutants, we used microarrays to study whether either pol30-8, dot1 or the double mutant leads to changes in gene expression levels when compared to isogenic wild-type strains.

Publication Title

A common telomeric gene silencing assay is affected by nucleotide metabolism.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24327
Lack of Toll-like Receptor Signaling Improves Host Defense in Severe Septic Peritonitis in Severe Septic Peritonitis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

TLRs are considered important for innate immune responses that combat bacterial infections. Here, the role of TLRs in severe septic peritonitis using the colon ascendens stent peritonitis (CASP) model was examined. We demonstrate that mice deficient for MyD88 and TRIF had markedly reduced bacterial numbers both in peritoneal cavity and peripheral blood, indicating that bacterial clearance in this model is inhibited by TLR signals. Moreover, survival of Myd88-/-;TrifLps2/Lps2 mice was significantly improved. The lack of TLR signals prevented the excessive induction of inflammatory cytokines and of IL 10. Notably, the expression of IFN-gamma, which has an essential protective role in septic peritonitis, and of IFN-regulated genes including several p47 and p65 GTPases as well as IP 10 was independent of TLR signaling. These results provide evidence that, in severe septic peritonitis, TLR deficiency balances the innate immune response in a favorable manner by attenuating deleterious responses such as excessive cytokine release, while leaving intact protective IFN-gamma production.

Publication Title

Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE23711
Expression profiling of nhp6 mutants and wildtype yeast cells (Saccharomyces cerevisiae)
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The basic unit of genome packaging is the nucleosome, and nucleosomes have long been proposed to restrict DNA accessibility both to damage and to transcription. However, nucleosome number in cells was considered fixed, and no condition was described where nucleosome number was reduced. We show here that mammalian cells lacking High Mobility Group Box 1 protein (HMGB1) contain a reduced amount of core, linker and variant histones, and a correspondingly reduced number of nucleosomes. Yeast nhp6 mutants lacking NHP6A and B proteins, which are related to HMGB1, also have a reduced amount of histones and fewer nucleosomes. Nucleosome limitation in both mammalian and yeast cells increases the sensitivity of DNA to damage, increases transcription globally, and the relative expression of about 10% of genes. In yeast nhp6 cells the loss of more than one nucleosome in four does not affect the location of nucleosomes and their spacing, but nucleosomal occupancy. The decrease in nucleosomal occupancy is non-uniform, and our results can be modelled assuming that different nucleosomal sites compete for the available histones: sites with high affinity are almost always packaged into nucleosomes both in wt and nucleosome-depleted cells, whereas sites with low affinity are less frequently packaged in nucleosome-depleted cells. We suggest that by modulating the occupancy of nucleosomes histone availability may constitute a novel layer of epigenetic regulation.

Publication Title

Substantial histone reduction modulates genomewide nucleosomal occupancy and global transcriptional output.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE110545
Transcriptome data from Eomes-overexpressing Th17 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Th17 cells were sorted ex vivo from PB of healthy donors as CD4+CD161+CCR6+CXCR3-. Following, cells were transduced with a lentiviral vector carrying the Eomes gene or with an empty vector. Infected cells were then enriched by MACS separation using the reporter gene NGFR as selection marker. Finally, cells were frozen for RNA analysis.

Publication Title

Eomes controls the development of Th17-derived (non-classic) Th1 cells during chronic inflammation.

Sample Metadata Fields

Cell line

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accession-icon GSE31189
Molecular Biomarker Signature for Bladder Cancer Detection
  • organism-icon Homo sapiens
  • sample-icon 88 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study we applied differential gene expression analysis to exfoliated human urothelia obtained from patients of known bladder disease status. Selected targets from the microarray data were validated in an independent set of samples using a quantitative PCR approach.

Publication Title

A candidate molecular biomarker panel for the detection of bladder cancer.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE24917
Genome wide gene expression profiles of Drosophila l(3)mbt larval brains and cultured tumors
  • organism-icon Drosophila melanogaster
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Mutants in the Drosophila gene lethal (3) malignant brain tumor cause malignant growth in the larval brain. This data shows the changes in gene expression profile associated to mutations in l(3)mbt, both in situ in third instar larval brains and in tumors cultured for 1 5 and 10 (T1, T5, T10) rounds of allograft culture

Publication Title

Ectopic expression of germline genes drives malignant brain tumor growth in Drosophila.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP031504
RNA-seq transcriptome profiling of equine inner cell mass and trophectoderm
  • organism-icon Equus caballus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transcriptomic analysis of ICM and TE from in vivo-derived equine blastocysts using Illumina sequencing technology Overall design: RNA was extracted from individual equine blastocyst ICM and TE (Arcturus Picopure), cDNA was synthesized and amplified (Nugen Ovation V2) and indexed libraries were created for sequencing (TruSeq DNA V1)

Publication Title

RNA-seq transcriptome profiling of equine inner cell mass and trophectoderm.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP066449
Homo sapiens Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

BJAB cells over expressing KSHV PAN RNA

Publication Title

Regulation of viral and cellular gene expression by Kaposi's sarcoma-associated herpesvirus polyadenylated nuclear RNA.

Sample Metadata Fields

No sample metadata fields

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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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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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