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accession-icon GSE64603
Blood transcriptomes of chronic HCV patients four years after therapy-induced viral clearance
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Little is known on the immune status in liver and blood of chronic HCV patients long after therapy-induced viral clearance. In this study, we demonstrate that 4 years after clearance, regulation of HCV-specific immunity in blood by regulatory T-cells (Treg) and the immunosuppressive cytokines IL-10 and TGF- is still ongoing. Importantly, sampling of the liver 4 years after clearance shows that intrahepatic Treg are still present in all patients, suggesting that liver T-cells remain regulated. Identifying mechanisms that regulate HCV-specific memory T-cell responses after clearance is highly relevant for the development of protective vaccines, especially in patients at high-risk of reinfection.

Publication Title

The Intrahepatic T Cell Compartment Does Not Normalize Years After Therapy-Induced Hepatitis C Virus Eradication.

Sample Metadata Fields

Sex, Specimen part, Race

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accession-icon GSE46243
Role of EGR2 transcription factor in T cell anergy
  • organism-icon Mus musculus
  • sample-icon 12 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

Egr2-dependent gene expression profiling and ChIP-Seq reveal novel biologic targets in T cell anergy.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE46242
Egr2-dependent expression in T cell anergy
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

T cell anergy is one of the mechanisms contributing to peripheral tolerance, particularly in the context of progressively growing tumors and in tolerogenic treatments promoting allograft acceptance. We recently reported that early growth response gene 2 (Egr2) is a critical transcription factor for the induction of anergy in vitro and in vivo, which was identified based on its ability to regulate the expression of inhibitory signaling molecules diacylglycerol kinase (DGK)-a and -z. We reasoned that other transcriptional targets of Egr2 might encode additional factors important for T cell anergy and immune regulation. Thus, we conducted two sets of genome-wide screens: gene expression profiling of wild type versus Egr2-deleted T cells treated under anergizing conditions, and a ChIP-Seq analysis to identify genes that bind Egr2 in anergic cells. Merging of these data sets revealed 49 targets that are directly regulated by Egr2. Among these are inhibitory signaling molecules previously reported to contribute to T cell anergy, but unexpectedly, also cell surface molecules and secreted factors, including lymphocyte-activation gene 3 (Lag3), Class-I-MHC-restricted T cell associated molecule (Crtam), Semaphorin 7A (Sema7A), and chemokine CCL1. These observations suggest that anergic T cells might not simply be functionally inert, and may have additional functional properties oriented towards other cellular components of the immune system.

Publication Title

Egr2-dependent gene expression profiling and ChIP-Seq reveal novel biologic targets in T cell anergy.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE51382
Retroviral overexpression or siRNA mediated knockdown of FOXP1 in DLBCL cell lines and primary human B cells
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To provide insight into the role of and target genes of the transcription factor FOXP1 in mature human B cells and in B cell non-Hodkgin lymhomas, we performed gene expression microarray studies, upon ectopic overexpression or silencing of FOXP1 in these cells.

Publication Title

FOXP1 directly represses transcription of proapoptotic genes and cooperates with NF-κB to promote survival of human B cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP044678
RNA-seq analysis of MEF cell transcriptome after Salmonella Typhimurium infection
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We infected Mouse Embryonic Fibroblast and cultured them in anchorage independent conditions to study tranformation induced by the bacterium. We cultured these transformed cells multiple rounds in the presence of Ciprofloxacin to remove intracellular Salmonella after transformation occured. By doing RNA sequencing we indentified genes of which expression was altered upon infection. This helps us to understand how Salmonella alters the host cell, resulting in transformation Overall design: We Cultered two biological duplicates of infected MEF cells, which we compared to a non transformed MEF control sample

Publication Title

Salmonella Manipulation of Host Signaling Pathways Provokes Cellular Transformation Associated with Gallbladder Carcinoma.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP162873
RNA sequencing in healthy controls, intermittent claudicant, and CLI patient skeletal muscle
  • organism-icon Homo sapiens
  • sample-icon 50 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Gastrocnemius muscle biopsies were obtained from 15 health older adults without peripheral artery disease (PAD), 20 PAD patients with intermittent claudication, and 16 patients with critical limb ischemia undergoing limb amputation. Gene expression analysis was performed using RNA sequencing analysis. Overall design: Examination of gene expression differences across the clinical spectrum of PAD (healthy vs. claudicant vs. critical limb ischemia)

Publication Title

Extensive skeletal muscle cell mitochondriopathy distinguishes critical limb ischemia patients from claudicants.

Sample Metadata Fields

Specimen part, Disease, Subject

View Samples
accession-icon GSE9482
GAL-NMD2
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

The goal of this set of experiments was to identify transcripts that are differentially expressed upon reactivation of NMD in an nmd2::HIS3 strain by galactose-induced expression of the NMD2 gene.

Publication Title

Association of yeast Upf1p with direct substrates of the NMD pathway.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE18113
Expression data from Human MicroVascular Endothelial Cells (HMVECS)
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The activation of endothelium by tumor cells is one of the main steps by tumor metastasis. The role of the blood components (platelets and leukocytes) in this process remain unclear.

Publication Title

Selectin-mediated activation of endothelial cells induces expression of CCL5 and promotes metastasis through recruitment of monocytes.

Sample Metadata Fields

Specimen part

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accession-icon SRP108720
RNA-Seq of polysome profiling fractions and whole cell lysates of UVB-irradiated N-TERT keratinocytes
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

In response to UVB irradiation, human keratinocytes transiently block cell cycle progression to allow ample time for DNA repair and cell fate determination. These cellular processes are important for evading the initiation of carcinogenesis in skin. We previously showed that repression of mRNA translation initiation through phosphorylation of eIF2a (eIF2a-P) protects keratinocytes from UVB-induced apoptosis. In this study, we elucidate the mechanism of eIF2a-P cytoprotection in response to UVB. Loss of eIF2a-P induced by UVB diminished G1 arrest, DNA repair rate, and cellular senescence coincident with enhanced cell death in human keratinocytes. Genome-wide translation analyses revealed that the mechanism for these critical changes directed by eIF2a-P involved induced expression of CDKN1A encoding p21 protein. p21 is a major regulator of the cell cycle, and we show that human CDKN1A mRNA splice variant 4 is preferentially translated by eIF2a-P during stress in a mechanism mediated in part by upstream ORFs situated in the 5'-leader of CDKN1A mRNA. We conclude that eIF2a-P is cytoprotective in response to UVB by a mechanism featuring translation of a specific splice variant of CDKN1A that facilitates G1 arrest and subsequent DNA repair. Overall design: Untreated and irradiated N-TERT keratinocytes are split into 3 groups: monosome fraction, polysome fraction, and whole cell lysate. N=3.

Publication Title

Translational control of a human <i>CDKN1A</i> mRNA splice variant regulates the fate of UVB-irradiated human keratinocytes.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE9486
Upf1p-associated transcripts in S. cerevisiae
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

The goal of this experiment was to identify transcripts associated with the S. cerevisiae Upf1 protein.

Publication Title

Association of yeast Upf1p with direct substrates of the NMD pathway.

Sample Metadata Fields

No sample metadata fields

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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