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accession-icon GSE22853
Expression data from human Ea.hy926 cells in response to epoxomicin and in dependency of TCF11 presence
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Coordinated regulation of the ubiquitin-proteasome system is crucial for the cell to adjust its protein degradation capacity to changing proteolytic requirements. The transcription factor TCF11 has been identified as a regulator for 26S-proteasome formation in human cells to compensate for reduced proteolytic activity. To expand the current knowledge of other UPS-related TCF11 target genes in response to epoxomicin, we performed microarray analyses of cells exposed to epoxomicin and with or without depletion of TCF11.

Publication Title

Proteasomal degradation is transcriptionally controlled by TCF11 via an ERAD-dependent feedback loop.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE10316
Monocyte-derived dendritic cells stimulated with LPS, Poly(I:C), CD40L or a combination of IL-1-b, IL-6, TNF-a and PGE2
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The ubiquitin proteasome system (UPS) is known to possess important regulatory functions in the immune response. To gain a better and first comprehensive insight into the mechanisms underlying the conversion of immature to mature DC in terms of the expression of UPS related genes, we undertook a comparative gene expression profiling during DC maturation in response to four different prototypic maturation stimuli.

Publication Title

Maturation of human dendritic cells is accompanied by functional remodelling of the ubiquitin-proteasome system.

Sample Metadata Fields

No sample metadata fields

View Samples
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

View Samples
accession-icon GSE50736
TEL-AML1 (ETV6-RUNX1) in B-cells and leukemia
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The impact of TEL-AML1 (ETV6-RUNX1) expression in precursor B cells and implications for leukaemia using three different genome-wide screening methods.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Cell line

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accession-icon GSE75929
Expression data from UKRV-Mel-15a melanoma-derived clones resistant to cytolysis mediated by Melan-A/MART1 (26-35) cytotoxic T lymphocytes (CTL).
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Efficient processing of target antigens by the ubiquitin-proteasome-system (UPS) is essential for treatment of cancers by T cell therapies. However, immune escape due to impaired expression of IFN--inducible components of the antigen presentation machinery and consequent inefficient processing of HLA-dependent tumor epitopes can be one important reason for failure of such therapies. Here, we show that repeated short-term co-cultures of Melan-A/MART-1 tumor antigen-expressing melanoma cells with Melan-A/MART-1 (26-35)-specific CTL led to the generation of clones resistant to CTL-mediated cell death. To determine which of the UPS components and its associated pathways was responsible for CTL escape; three UKRV-Mel-15a clones were subjected to microarray gene expression analysis.

Publication Title

Exposure to Melan-A/MART-126-35 tumor epitope specific CD8(+)T cells reveals immune escape by affecting the ubiquitin-proteasome system (UPS).

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE50735
TEL-AML1 (ETV6-RUNX1) in B-cells and leukemia (part 6)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein.

Publication Title

The impact of TEL-AML1 (ETV6-RUNX1) expression in precursor B cells and implications for leukaemia using three different genome-wide screening methods.

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP066354
Pregnacy-induced regulation of islet proteins
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report pregnacy-induced changes at the RNA level using RNAseq Overall design: Comparison of RNA transcript of islets isolated from 5 control and 5 pregnant animals at gestational day 14.5

Publication Title

Research Resource: A Dual Proteomic Approach Identifies Regulated Islet Proteins During β-Cell Mass Expansion In Vivo.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE107033
Endothelial gene expression analysis
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE107032
Endothelial gene expression analysis after silencing LOXL2 using siRNAs
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Impaired or excessive growth of endothelial cells contributes to several diseases. However, the functional involvement of regulatory long non-coding RNAs in these processes is not well defined. Here we show that the long non-coding antisense transcript of GATA6 (GATA6-AS) interacts with the epigenetic regulator LOXL2 to regulates endothelial gene expression via changes in histone methylation. Using RNA deep sequencing, we find that GATA6-AS is up-regulated in endothelial cells during hypoxia. Silencing of GATA6-AS diminishes TGF-2-induced endothelial-mesenchymal transition in vitro and promotes formation of blood vessels in mice. We identify LOXL2, known to remove activating H3K4me3 chromatin marks, as a GATA6-AS-associated protein, and reveal a set of angiogenesis-related genes that are inversely regulated by LOXL2 and GATA6-AS silencing. As GATA6-AS silencing reduces H3K4me3 methylation of two of these genes, periostin and cyclooxygenase-2, we conclude that GATA6-AS acts as negative regulator of nuclear LOXL2 function.

Publication Title

The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE107031
Endothelial gene expression analysis after silencing the lncRNA GATA6-AS using LNA GapmeRs.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Impaired or excessive growth of endothelial cells contributes to several diseases. However, the functional involvement of regulatory long non-coding RNAs in these processes is not well defined. Here we show that the long non-coding antisense transcript of GATA6 (GATA6-AS) interacts with the epigenetic regulator LOXL2 to regulates endothelial gene expression via changes in histone methylation. Using RNA deep sequencing, we find that GATA6-AS is up-regulated in endothelial cells during hypoxia. Silencing of GATA6-AS diminishes TGF-2-induced endothelial-mesenchymal transition in vitro and promotes formation of blood vessels in mice. We identify LOXL2, known to remove activating H3K4me3 chromatin marks, as a GATA6-AS-associated protein, and reveal a set of angiogenesis-related genes that are inversely regulated by LOXL2 and GATA6-AS silencing. As GATA6-AS silencing reduces H3K4me3 methylation of two of these genes, periostin and cyclooxygenase-2, we conclude that GATA6-AS acts as negative regulator of nuclear LOXL2 function.

Publication Title

The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.

Sample Metadata Fields

No sample metadata fields

View Samples

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)

fund-icon Fund the CCDL

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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