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accession-icon SRP167977
Gene expression profile in FTSEC cells (FT190 and FT194 cell lines) transduced with shRNA to knockdown RNF20 or with control shRNA using RNA-seq.
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We identified that downregulation of RNF20/H2Bub1 is involved in HGSOC progression through altering key immune signaling pathways. The goal of this RNA-seq is to analyze gene expression profile in FTSEC cells (FT190 and FT194 cell lines) with RNF20 knockdown (shRNF20) or control shRNA. Integrating the data from ATAC-seq for same samples, we observed that expression of immune signaling pathways have significantly changed by RNF20/H2Bub1 downregulation. Overall design: mRNA profiles of FT190 and FT194 shRNF20 (RNF20 knockdown) or control shRNA cells were generated by deep sequencing using Illumina HiSeq 2500, in triplicate.

Publication Title

Early Loss of Histone H2B Monoubiquitylation Alters Chromatin Accessibility and Activates Key Immune Pathways That Facilitate Progression of Ovarian Cancer.

Sample Metadata Fields

Subject

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accession-icon SRP165279
Early response to loss of Argonaute proteins in embryonic stem cells activates the Tgf-ß/Smad Transcriptional Network [mRNA-Seq: DicerDgcr8_KOs]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Argonaute (Ago) proteins, which act in post-transcriptional gene regulation directed by small RNAs, are vital for normal stem cell biology. Here we report the genomic characterization of stable Ago-deficient mouse embryonic stem cells (mESC) and determine the direct, primary and system level response to loss of Ago-mediated regulation. We find mESCs lacking all four Ago proteins are viable, do not repress microRNA (miRNA)-targeted cellular RNAs, and show distinctive gene network signatures. Profiling of RNA expression and epigenetic activity in an Ago mutant genetic series indicates that early responses to Ago loss are driven by transcriptional regulatory networks, in particular the Tgf-ß/Smad transcriptional network. This finding is confirmed using a time course analysis of Ago depletion and Ago rescue experiments. Detailed analysis places Tgf-ß/Smad activation upstream of cell cycle regulator activation, such as Cdkn1a, and repression of the c-Myc transcriptional network. The Tgf-ß/Smad pathway is directly controlled by multiple low-affinity miRNA interactions with Tgf-ß/Activin receptor mRNAs and receptor-mediated activation is required for Tgf-ß/Smad target induction with Ago loss. Our characterization reveals the interplay of post-transcriptional regulatory pathways with transcriptional networks in maintaining cell state and likely coordinating cell state transitions. Overall design: mRNA seq from stable genetic Dicer and Dgcr8 mutant mouse embryonic stem cells.

Publication Title

Temporal Control of the TGF-β Signaling Network by Mouse ESC MicroRNA Targets of Different Affinities.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP095644
Gene expression profiling of histone deacetylase inhibition in triple-negative breast cancer
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Analysis of changes in gene expression levels after after prolonged exposure of triple-negative breast cancer cell lines to low doses of Panobinostat (LBH589), a pan-histone deacetylase inhibitor. Overall design: RNA-sequencing was performed after 96 hours and 4 weeks of incubation 10 nmol/L of LBH589 of two triple-negative breast cancer cell lines (HCC1806 and MDA-MB-231). All the expreiments were performed in biological triplicates

Publication Title

Genome-wide chromatin accessibility, DNA methylation and gene expression analysis of histone deacetylase inhibition in triple-negative breast cancer.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP031831
The dsRBP and inactive editor, ADR-1, utilizes dsRNA binding to regulate A-to-I RNA editing across the C. elegans transcriptome
  • organism-icon Caenorhabditis elegans
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II, Illumina HiSeq 2000

Description

Purpose: The purpose of this experiment is to expand the repertoire of C. elegans edited transcripts and identify the roles of ADR-1 as indirect regulator of editing and ADR-2 as the only active deaminase in vivo. Methods: Strand-specific RNA sequencing of wild-type and adr mutant worms, followed by a novel RNA variant calling and comparative analysis pipeline. Results: Despite lacking deaminase function, ADR-1 affects editing of over 60 adenosines within the 3’ UTRs of 16 different mRNAs. Furthermore, ADR-1 interacts directly with ADR-2 substrates, even in the absence of ADR-2; and mutations within its dsRNA binding domains abolished both binding and editing regulation. Conclusions: ADR-1 acts as a major regulator of editing by binding ADR-2 substrates in vivo and raises the possibility that other dsRNA binding proteins, including the inactive human ADARs, regulate RNA editing by deaminase-independent mechanisms. Overall design: Strand-specific RNA sequencing of wild-type and adr mutant worms, followed by a novel RNA variant calling and comparative analysis pipeline.

Publication Title

The dsRBP and inactive editor ADR-1 utilizes dsRNA binding to regulate A-to-I RNA editing across the C. elegans transcriptome.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE67088
Vemurafenib resistance selects for highly malignant brain and lung-metastasizing melanoma cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

V600E being the most common mutation in BRAF, leads to constitutive activation of the MAPK signaling pathway. The majority of V600E BRAF positive melanoma patients treated with the BRAF inhibitor vemurafenib showed initial good clinical responses but relapsed due to acquired resistance to the drug. The aim of the present study was to identify possible biomarkers associated with the emergence of drug resistant melanoma cells. To this end we analyzed the differential gene expression of vemurafenib-sensitive and vemurafenib resistant brain and lung metastasizing melanoma cells.

Publication Title

Vemurafenib resistance selects for highly malignant brain and lung-metastasizing melanoma cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP091793
Mechanism of Induction of Mouse Breast Cancer by Non-coding Heterochromatic RNAs
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Heterochromatic non-coding RNAs induce breast tumor formation in mice by interacting with BRCA1-associated proteins functioning in the DNA damage response. Overall design: mouse tumor mRNA profiles using ribosomal mRNA depletion

Publication Title

Heterochromatin-Encoded Satellite RNAs Induce Breast Cancer.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE45648
Anti-BRAF mutation drug resistance enhances EGFR expression in melanomas [expression profiling]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We treated melanoma cells with BRAF mutation with BRAF inhibitor and screened for BRAF inhibitor resistant cells. We extracted total mRNA from parental cells and resistant cell lines. We compared their expression by carried out Affymetrix Huex 1.0 ST expression array.

Publication Title

Epigenetic changes of EGFR have an important role in BRAF inhibitor-resistant cutaneous melanomas.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP014671
LIN28 binds messenger RNAs at GGAGA motifs and regulates splicing factor abundance (HTS)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer, Illumina Genome Analyzer II

Description

LIN28 is a conserved RNA binding protein implicated in pluripotency, reprogramming and oncogenesis. Previously shown to act primarily by blocking let-7 microRNA (miRNA) biogenesis, here we elucidate distinct roles of LIN28 regulation via its direct messenger RNA (mRNA) targets. Through cross-linking and immunoprecipitation coupled with high-throughput sequencing (CLIP-seq) in human embryonic stem cells and somatic cells expressing exogenous LIN28, we have defined discrete LIN28 binding sites in a quarter of human transcripts. These sites revealed that LIN28 binds to GGAGA sequences enriched within loop structures in mRNAs, reminiscent of its interaction with let-7 miRNA precursors. Among LIN28 mRNA targets, we found evidence for LIN28 autoregulation and also direct but differing effects on the protein abundance of splicing regulators in somatic and pluripotent stem cells. Splicing-sensitive microarrays demonstrated that exogenous LIN28 expression causes widespread downstream alternative splicing changes. These findings identify important regulatory functions of LIN28 via direct mRNA interactions. Overall design: CLIP-seq for LIN28-V5 in stable human Flp-In-293 cells, and LIN28 in hES cells; strand-specific mRNA-seq for uninfected, control KD, and LIN28 KD human H9 ES cells; and strand-specific smallRNA-seq for uninfected, control KD, and LIN28 KD human H9 ES cells.

Publication Title

LIN28 binds messenger RNAs at GGAGA motifs and regulates splicing factor abundance.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon GSE59210
Genome wide expression analysis of bone marrow derived macrophage cells (BMDMs) stimulated with IFNg and effect of Batf2 knockdown in BMDMs stimulated with IFNg
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Batf2/Irf1 induces inflammatory responses in classically activated macrophages, lipopolysaccharides, and mycobacterial infection.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE59207
Genome wide expession analysis of mouse bone marrow derive macrophage (Bmdm) cell stimulated with IFNg
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Bmdm cells were differentiated for 10 days and harvested and culture in six well plate followed by cytokine stimulation

Publication Title

Batf2/Irf1 induces inflammatory responses in classically activated macrophages, lipopolysaccharides, and mycobacterial infection.

Sample Metadata Fields

Sex, Specimen part

View Samples
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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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