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accession-icon SRP026382
A miR-155-ruled microRNA hierarchy in dendritic cell maturation and macrophage activation
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in many cellular pathways. MiRNAs associate with members of the Argonaute (Ago) protein family and bind to partially complementary sequences on mRNAs and induce translational repression or mRNA decay. MiRNA expression can be controlled by transcription factors and can therefore be cell type- or tissue-specific. Here we have analyzed miRNA expression profiles in murine monocyte-derived dendritic cells (DCs) and macrophages upon stimulation with LPS, LDL, eLDL and oxLDL to identify not only stimuli-specific miRNA, but also to identify a hierarchical miRNA system involving miR-155. For this, miR-155 knockout dendritic cells and macrophages were also sequenced using the same stimuli. Overall design: Sequencing of murine monocyte-derived dendritic cells and macrophages (each wild type and miR-155 knock out cells) matured and stimulated, respectively, by LPS, oxLDL, eLDL or LDL.

Publication Title

A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE98062
Gene expression in non-adherent MDA-MB-468 subpopulation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Plasticity between adhesive and less-adhesive states is important for mammalian cell behaviour. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of MDA-MB-468 breast carcinoma cells which grows in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices.

Publication Title

A dual phenotype of MDA-MB-468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP069880
Posttranscriptional control of the neutrophil transcriptome by tristetraprolin promotes neutrophil apoptosis and compromises host antimicrobial defense
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Posttranscriptional regulation of mRNA levels in neutrophils and its consequences for immune responses are unexplored. By employing profiling of the neutrophil transcriptome we show that the mRNA-destabilizing protein tristetraprolin (TTP) limits the expression of hundreds of genes, including genes negatively regulating apoptosis. Elicited TTP-deficient neutrophils exhibited reduced apoptosis and were increased in numbers. The anti-apoptotic protein Mcl-1 was elevated in TTP-deficient neutrophils and Mcl1 mRNA was bound and destabilized by TTP. Ablation of TTP in macrophages and neutrophils resulted in an improved defense and survival of mice during invasive infection with Streptococcus pyogenes. Mice lacking myeloid TTP prevented dissemination of bacteria and efficiently blunted systemic disease by massive but controlled neutrophil deployment. These data identify posttranscriptional control by TTP to restrict neutrophils and antimicrobial defense. Overall design: WT and TTPKO peritoneal neutrophils stimulated with LPS for 4 h. Each condition analyzed in three replicates

Publication Title

The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.

Sample Metadata Fields

Subject

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accession-icon GSE53469
Epigenetic regulations in the IFN signalling pathway: IFN-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip, Illumina MouseWG-6 v2.0 R2 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE53467
Epigenetic regulations in the IFN signalling pathway: IFN-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [TC1A9_IFN]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip, Illumina MouseWG-6 v2.0 R2 expression beadchip

Description

Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFN. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFN treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFN acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.

Publication Title

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE53465
Epigenetic regulations in the IFN signalling pathway: IFN-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [RVPC3_DAC]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFN. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFN treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFN acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.

Publication Title

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE53466
Epigenetic regulations in the IFN signalling pathway: IFN-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes [TC1A9_DAC]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Reversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFN. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFN treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFN acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.

Publication Title

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP050246
Effect of REST-003 downregulation on cancer invasiveness in MDA-MB-231 cells using RNA-sequencing (RNA-seq) analysis .
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Fifty six genes from DESeq were differentially expressed in the treated versus control samples. More than 20% were related to immune, defense, wounding and inflammatory responses Overall design: Downregulation of REST-003 using siRNAs in MDA-MB-231 cells; we used siRNA against REST-003, as REST-003 may control invasiveness. We transfected si-Control (scramble) or si-REST-003 in MDA-MB-231: duplicate of both (total 4 samples).

Publication Title

Non-coding RNAs derived from an alternatively spliced REST transcript (REST-003) regulate breast cancer invasiveness.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37748
Genotoxic alterations of cord blood cells in newborns exposed in utero to a zidovudine-based antiretroviral combination
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Zidovudine remains the cornerstone drug for prophylaxis to prevent mother-to-child HIV-1 transmission. A mild but long-lasting hematological multilineage defect is observed in children exposed in utero.

Publication Title

Genotoxic signature in cord blood cells of newborns exposed in utero to a Zidovudine-based antiretroviral combination.

Sample Metadata Fields

Specimen part, Treatment

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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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