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accession-icon GSE87483
Dnmt3a restrains mast cell inflammatory responses
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

By utilizing mast cells lacking Dnmt3a, we found that this enzyme is involved in restraining mast cell responses to stimuli, both in vitro and in vivo.

Publication Title

<i>Dnmt3a</i> restrains mast cell inflammatory responses.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE94380
Gene expression data of Peyer's patch conventional dendritic cells and macrophages at steady state and under TLR7 ligand stimulation
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The initiation of the mucosal immune response in Peyers patch (PP) relies on the sampling, processing and efficient presentation of foreign antigens by dendritic cells (DC). PP DC encompass five subsets, among which CD11b+ conventional DC (cDC) and LysoDC have distinct progenitors and functions but share many cell surface markers. This has previously led to confusion between these two subsets. In addition, another PP DC subset, termed double-negative (DN), remains poorly characterized. Here, we have studied the genetic relatedness of the different subsets of PP cDC at steady state and under TLR7 ligand stimulation. We also provide the transcriptional profiles of subepithelial TIM-4- and interfollicular TIM-4+ macrophages.

Publication Title

Distribution, location, and transcriptional profile of Peyer's patch conventional DC subsets at steady state and under TLR7 ligand stimulation.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE62064
Radial glia require PDGFD/PDGFRB signaling in human but not mouse neocortex
  • organism-icon Homo sapiens
  • sample-icon 87 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of gene expression over serial 150um sections of a single gestational week 14.5 human neocortical specimen. The hypothesis tested with this dataset was that a transcriptional signature of radial glia (neural stem cells) could be isolated via unsupervised gene coexpression analysis due to variation in the abundance of this cell type from section to section. This dataset is the first of its kind generated using this method (Gene Coexpression Analysis of Serial Sections, or GCASS).

Publication Title

Radial glia require PDGFD-PDGFRβ signalling in human but not mouse neocortex.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE53679
Pax3 and Zic1 trigger the early neural crest gene regulatory network by the direct activation of multiple key neural crest specifiers
  • organism-icon Xenopus laevis
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2), Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Pax3 and Zic1 trigger the early neural crest gene regulatory network by the direct activation of multiple key neural crest specifiers.

Sample Metadata Fields

Specimen part

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accession-icon GSE53677
Pax3 and Zic1 trigger the early neural crest gene regulatory network by the direct activation of multiple key neural crest specifiers [X_laevis_2]
  • organism-icon Xenopus laevis
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome 2.0 Array (xlaevis2)

Description

Neural crest development is orchestrated by a complex and still poorly understood gene regulatory network. Premigratory neural crest is induced at the lateral border of the neural plate by the combined action of signaling molecules and transcription factors such as AP2, Gbx2, Pax3 and Zic1. Among them, Pax3 and Zic1 are both necessary and sufficient to trigger a complete neural crest developmental program. However, their gene targets in the neural crest regulatory network remain unknown. Here, through a transcriptome analysis of frog microdissected neural border, we identified an extended gene signature for the premigratory neural crest, and we defined novel potential members of the regulatory network. This signature includes 34 novel genes, as well as 44 known genes expressed at the neural border. Using another microarray analysis which combined Pax3 and Zic1 gain-of-function and protein translation blockade, we uncovered 25 Pax3 and Zic1 direct targets within this signature. We demonstrated that the neural border specifiers Pax3 and Zic1 are direct upstream regulators of neural crest specifiers Snail1/2, Foxd3, Twist1, and Tfap2b. In addition, they may modulate the transcriptional output of multiple signaling pathways involved in neural crest development (Wnt, Retinoic Acid) through the induction of key pathway regulators (Axin2 and Cyp26c1). We also found that Pax3 could maintain its own expression through a positive autoregulatory feedback loop. These hierarchical inductions, feedback loops, and pathway modulation provide novel tools to understand the neural crest induction network.

Publication Title

Pax3 and Zic1 trigger the early neural crest gene regulatory network by the direct activation of multiple key neural crest specifiers.

Sample Metadata Fields

Specimen part

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accession-icon GSE53678
Pax3 and Zic1 trigger the early neural crest gene regulatory network by the direct activation of multiple key neural crest specifiers [Xenopus_laevis]
  • organism-icon Xenopus laevis
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

Neural crest development is orchestrated by a complex and still poorly understood gene regulatory network. Premigratory neural crest is induced at the lateral border of the neural plate by the combined action of signaling molecules and transcription factors such as AP2, Gbx2, Pax3 and Zic1. Among them, Pax3 and Zic1 are both necessary and sufficient to trigger a complete neural crest developmental program. However, their gene targets in the neural crest regulatory network remain unknown. Here, through a transcriptome analysis of frog microdissected neural border, we identified an extended gene signature for the premigratory neural crest, and we defined novel potential members of the regulatory network. This signature includes 34 novel genes, as well as 44 known genes expressed at the neural border. Using another microarray analysis which combined Pax3 and Zic1 gain-of-function and protein translation blockade, we uncovered 25 Pax3 and Zic1 direct targets within this signature. We demonstrated that the neural border specifiers Pax3 and Zic1 are direct upstream regulators of neural crest specifiers Snail1/2, Foxd3, Twist1, and Tfap2b. In addition, they may modulate the transcriptional output of multiple signaling pathways involved in neural crest development (Wnt, Retinoic Acid) through the induction of key pathway regulators (Axin2 and Cyp26c1). We also found that Pax3 could maintain its own expression through a positive autoregulatory feedback loop. These hierarchical inductions, feedback loops, and pathway modulation provide novel tools to understand the neural crest induction network.

Publication Title

Pax3 and Zic1 trigger the early neural crest gene regulatory network by the direct activation of multiple key neural crest specifiers.

Sample Metadata Fields

Specimen part

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accession-icon GSE107876
Dissecting cell-intrinsic roles of MyD88 and IFN-I signalling in pDC responses to a viral infection in vivo
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Plasmacytoid dendritic cells (pDC) are the major source of type I interferons (IFN-I) during viral infections, in response to triggering of endosomal Toll Like Receptors (TLR) 7 or 9 by viral single-stranded RNA or unmethylated CpG DNA, respectively. IFN-I production in pDC occurs in specialized endosomes encompassing preformed signaling complexes of TLR7 or 9 with their adaptor molecule MyD88 and the transcription factor interferon regulatory factor 7 (IRF7). The triggering of TLR leads to IRF7 phosphorylation, nuclear translocation and binding to the promoters of the genes encoding IFN-I to initiate their transcription. pDC express uniquely high levels of IRF7 at steady state and this expression is further enhanced by positive IFN-I feedback signaling during viral infections. However, the specific cell-intrinsic roles of MyD88 versus IFN-I signaling in pDC responses to a viral infection have not been rigorously dissected. To achieve this aim, we generated mixed bone marrow chimera mice (MBMC) allowing to rigorously compare the gene expression profiles of WT versus Ifnar1-KO or MyD88-KO pDC isolated from the same animals at steady state or after infection with the mouse cytomegalovirus (MCMV). Our results indicate that, in vivo during MCMV infection, pDC undergo a major transcriptional reprogramming, under combined instruction of IFN-I, IFN- and direct TLR triggering. However, these different stimuli drive specific, largely distinct, gene expression programs. We rigorously determined which gene modules require cell-intrinsic IFN-I signaling for their induction in pDC during a physiological viral infection in vivo. We delineated non-redundant versus shared versus antagonistic responses with IFN-. We demonstrated that cell-intrinsic IFN-I responsiveness is dispensable for induction of the expression of all IFN-I/III genes and many cytokines or chemokines in pDC during MCMV infection, contrary to MyD88 signaling.

Publication Title

Molecular dissection of plasmacytoid dendritic cell activation <i>in vivo</i> during a viral infection.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE115450
Alignment of different types of resting or murine cytomegalovirus-activated mononuclear phagocytes across different datasets
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The goal of this experiment was to use global gene expression profiling to assess the global genetic reprogramming of different types of splenic mononuclear phagocytes early after MCMV infection in vivo. This study includes new samples (GSM3178486-GSM3178497; available below) profiling splenic CD11b+ conventional dendritic cells (cDC2), classical monocytes (cMo) and red pulp macrophages (RPM) from untreated or day 1.5 MCMV-infected mice together with re-analysis of previously published data in order to examine the similarities in the pDC gene expression profiles across datasets.

Publication Title

Molecular dissection of plasmacytoid dendritic cell activation <i>in vivo</i> during a viral infection.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP091504
High activity of a broad panel of housekeeping and tissue-specific cis-regulatory elements depends on a subset of ETS proteins
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The genomic repertoire of enhancers and promoters that control the transcriptional output of terminally differentiated cells includes cell type-specific and housekeeping elements. Whether the constitutive activity of these two groups of cis-regulatory elements relies on entirely distinct or instead shared regulators is unknown. By dissecting the cis-regulatory repertoire of macrophages, we found that the ELF subfamily of ETS proteins selectively bound within 60 bp from the transcription start sites of highly active housekeeping genes. ELFs also bound constitutively active, but not poised macrophage-specific enhancers and promoters. The role of ELFs in promoting constitutive transcription is suggested by multiple evidences: ELF sites enabled transcriptional activation by endogenous and minimal synthetic promoters; ELF recruitment was stabilized by the transcriptional machinery, and ELF proteins mediated recruitment of transcriptional and chromatin regulators to core promoters. These data indicate that a distinct subfamily of ETS proteins imparts high transcriptional activity to a broad range of housekeeping and tissue-specific cis-regulatory elements, which is consistent with the role of an ETS family ancestor in core promoter regulation in a lower eukaryote. Overall design: Nascent RNA sequencing of primary bone marrow-derived macrophages (BMDM) This series contains a re-analysis of GSM1880858 from GSE73021. The file MacroTFs_171-genes.fpkm_tracking.gz contains the FPKM values for this sample.

Publication Title

High constitutive activity of a broad panel of housekeeping and tissue-specific <i>cis</i>-regulatory elements depends on a subset of ETS proteins.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE49358
Genome-wide expression study of the CD11b+ subsets of dermal myeloid cells and their migratory counterparts in the draining lymph node
  • organism-icon Mus musculus
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Numerous CD11b+ myeloid cells are present within the dermis. They are very heterogeneous and can be divided in dermal DCs, tissue monocytes and tissue macrophages. At steady state, only CD11b+ DC migrate from the dermis to the skin draining lymph nodes whereas upon DNFB-induced inflammation, CD11b+ DC as well as dermal monocytes migrated to the lymph nodes. The objective of this study was to use gene expression profiling to rigorously identify the different subsets of dermal CD11b+ myeloid cells at steady state and upon inflammation and to characterize their functional potential.

Publication Title

Origins and functional specialization of macrophages and of conventional and monocyte-derived dendritic cells in mouse skin.

Sample Metadata Fields

Sex, Age, Specimen part

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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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