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accession-icon GSE47937
Gene expression changes due to influenza virus induced miRNAs
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The goal of this experiment was to determine gene expression changes during influenza A virus infection as the result of expression influenza virus inducible miRNAs in A549 cells.

Publication Title

Small RNA profiling of influenza A virus-infected cells identifies miR-449b as a regulator of histone deacetylase 1 and interferon beta.

Sample Metadata Fields

Cell line

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accession-icon SRP067490
RNAseq analysis of two independent stains of C57BL/6J-Plat-/- mice and wild-type C57BL/6J.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The ability to generate defined null mutations in mice revolutionized the analysis of gene function in mammals. However, gene-deficient mice generated by using 129-derived embryonic stem (ES) cells may carry large segments of 129 DNA, even when extensively backcrossed to reference strains, such as C57BL/6J, and this may confound interpretation of experiments performed in these mice. Tissue plasminogen activator (tPA), encoded by the PLAT gene, is a fibrinolytic serine protease that is widely expressed in the brain. A large number of neurological abnormalities have been reported in tPA-deficient mice. The studies here compare genes differentially expressed in the brains of Plat-/- mice from two independent Plat-/- mouse derivations to wild-type C57BL/6J mice. One strain denoted “Old” was constructed in ES cells from a 129 mouse and backcrossed extensively to C57BL/6J, and one denoted “New” Plat-/- mouse was constructed using zinc finger nucleases directly in the C57BL/6J-Plat-/- mouse strain. We identify a significant set of genes that are differentially expressed in the brains of Old Plat-/- mice that preferentially cluster in the vicinity of Plat on chromosome 8, apparently linked to more than 20 Mbp of DNA flanking Plat being of 129 origin. No such clustering is seen in the New Plat-/- mice. Overall design: Whole-transcriptome profiling of the cerebral cortex of wild-type control C57BL/6J mice and two independent Plat-/- mice strains on the C57BL/6J background.

Publication Title

Passenger mutations and aberrant gene expression in congenic tissue plasminogen activator-deficient mouse strains.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE25937
Gene expression in mouse liver depleted of HDAC3
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Liver-specific depletion of HDAC3 leads to liver steatosis (fatty liver), suggesting disregulation of lipid metabolism. This is correlated with changes in lipid metabolic gene expression.

Publication Title

A circadian rhythm orchestrated by histone deacetylase 3 controls hepatic lipid metabolism.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon SRP150723
Effect of BMP inhibition or stimulation of primary human keratinocytes
  • organism-icon Homo sapiens
  • sample-icon 59 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

BMP treatment induces expression of late differenitation genes in primary human keratinocytes. Overall design: RNA-seq analysis after treatment with EGFR inhibitor AG1478 with or without BMP27 or BMP inhibitor DMH1. each treatment and control was performed in triplicate

Publication Title

Single-Cell ID-seq Reveals Dynamic BMP Pathway Activation Upstream of the MAF/MAFB-Program in Epidermal Differentiation.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP163470
RNAseq of CD8+ and CD8- MAIT cells in human peripheral blood
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Mucosa-associated invariant T (MAIT) cells are unconventional innate-like T cells that recognize microbial riboflavin metabolites presented by the MHC class I-like protein MR1. Human MAIT cells predominantly express the CD8a co-receptor (CD8+), with a smaller subset lacking both CD4 and CD8 (DN). However, it is unclear if these two MAIT cell sub-populations distinguished by CD8a represent functionally distinct subsets. To address this, we investigated the phenotypic, transcriptional, and functional differences between CD8+ and DN MAIT cells using human samples from peripheral blood, mucosal tissues, and fetal tissues. Overall design: We FACS sorted CD8+ and CD8- MAIT cells from human peripheral blood and performed bulk RNAseq on these cells

Publication Title

The CD4<sup>-</sup>CD8<sup>-</sup> MAIT cell subpopulation is a functionally distinct subset developmentally related to the main CD8<sup>+</sup> MAIT cell pool.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP195743
Human Thoracic Duct Lymph Contains Circulatory Intermediates T Follicular Helper Cells [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

T follicular helper CD4 T cells (Tfh) provide requisite help to B cells in the germinal centers (GC) of lymphoid tissue. GC Tfh are identified by high expression of the chemokine receptor CXCR5 and the inhibitory molecule PD-1. Although more accessible, blood contains lower frequencies of CXCR5+ and PD-1+ cells that have been termed circulating Tfh (cTfh). However, it remains unclear whether GC Tfh exit lymphoid tissues and populate this cTfh pool. To examine exiting cells, we assessed the phenotype of Tfh present within the major conduit of efferent lymph from lymphoid tissues into blood, the human thoracic duct. Unlike blood, we consistently identified a CXCR5-Bright PD-1-Bright (CXCR5BrPD-1Br) Tfh population in thoracic duct lymph (TDL). These CXCR5BrPD-1Br TDL Tfh shared phenotypic and transcriptional similarities with GC Tfh. Moreover, components of the epigenetic profile of GC Tfh could be detected in CXCR5BrPD-1Br TDL Tfh, and the transcriptional imprint of this epigenetic signature was enriched in an activated cTfh subset known to contain vaccine-responding cells. Together with data showing shared TCR sequences between the CXCR5BrPD-1Br TDL Tfh and cTfh, these studies identify a population in TDL as a circulatory intermediate connecting the biology of Tfh in blood to Tfh in lymphoid tissue. Overall design: Transcriptional features of germinal center Tfh were detected in a population of Tfh in the efferent lymph of the human thoracic duct and can be traced to an activated subset of circulating Tfh in blood.

Publication Title

T follicular helper cells in human efferent lymph retain lymphoid characteristics.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE63848
Akt-Induced Mitochondrial Dysfunction in the Heart
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Sustained Akt activation induces cardiac hypertrophy (LVH), which may lead to heart failure. This study tested the hypothesis that Akt activation contributes to mitochondrial dysfunction in pathological LVH. Akt activation induced LVH and progressive repression of mitochondrial fatty acid oxidation (FAO) pathways. Preventing LVH by inhibiting mTOR failed to prevent the decline in mitochondrial function but glucose utilization was maintained. Akt activation represses expression of mitochondrial regulatory, FAO, and oxidative phosphorylation genes in vivo that correlate with the duration of Akt activation in part by reducing FOXO-mediated transcriptional activation of mitochondrial-targeted nuclear genes in concert with reduced signaling via PPAR/PGC-1 and other transcriptional regulators. In cultured myocytes Akt activation disrupted mitochondrial bioenergetics, which could be partially reversed by maintaining nuclear FOXO, but not by increasing PGC-1. Thus, although short-term Akt activation may be cardioprotective during ischemia by reducing mitochondrial metabolism and increasing glycolysis, long-term Akt activation in the adult heart contributes to pathological LVH in part by reducing mitochondrial oxidative capacity.

Publication Title

Enhanced cardiac Akt/protein kinase B signaling contributes to pathological cardiac hypertrophy in part by impairing mitochondrial function via transcriptional repression of mitochondrion-targeted nuclear genes.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP150759
Simultaneous quantification of antibody-RNA conjugates and the transcriptome from fixed cells by RAID
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Undifferentiated and differentiated Keratinocytes (AG1478 treated) were stained with antibody-RNA conjugates to measure protein-based diffrentiation changes in conjunction with single-cell transcriptomics. The cells were crosslinked and stained according to the RAID procedure to allow intracellular immunostaining. Antibodies used in this experiment are (TGM1, NOTCH1, KLK6, JAG1, phospho-RPS6, phospho-FAK). Overall design: Three 384 wells plates for untreated and Three 384 wells plates for AG1478 treated cells were processed for single cell transcriptomics

Publication Title

Combined quantification of intracellular (phospho-)proteins and transcriptomics from fixed single cells.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon SRP150624
Comparison of single-cell transcriptomics quality between unfixed cells and cells that were fixed and mock stained according to the RAID procedure
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Cell fixation, permeabilization and antibody staining of could have adverse effects on the quality of single cell transcriptomics data. To assess the effects of the RAID procedure, which includes such steps, we performed a direct comparison of single cell transcriptomics by CELseq2 using unfixed and RAID-processed cells. Quality measures (gene complexity, gene detection rate, average gene expression) were performed using 40000 samples UMI counts per cell. Overall design: Single cells were sorted in 96, wells plates. Per condition (unfixed or RAID) three sets (A,B,C) of 48 cells were processed with the CELseq2 protocol.

Publication Title

Combined quantification of intracellular (phospho-)proteins and transcriptomics from fixed single cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP150758
Simultaneous quantification of antibody-RNA conjugates and the transcriptome by single cell RNA-sequencing
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Undifferentiated and differentiated Keratinocytes (AG1478 treated) were stained with antibody-RNA conjugates (targeting EGFR and ITGA6) to measure protein-based differentiation changes in conjunction with single-cell transcriptomics. Overall design: Two 384 wells plates for untreated and two 384 wells plates for AG1478 treated cells were processed for single cell transcriptomics.

Publication Title

Combined quantification of intracellular (phospho-)proteins and transcriptomics from fixed single cells.

Sample Metadata Fields

Specimen part, Treatment, Subject

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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