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accession-icon GSE36009
Gene expression data from Wild Type and Nlrp10 deficient dendritic cells treated with or without LPS
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Nlrp10-deficient mice have a profound defect in helper T cell-driven immune responses. T cell priming is impaired due to a defect in the emigration of a dendritic cells from inflamed tissue and antigen transport to draining lymph nodes. DC chemotaxis to CCR7-dependent and independent ligands is intact in the absence of Nlrp10.

Publication Title

NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE38850
Expression profiling of mouse embryonic stem cells (ESCs) (cell line V6.5, 129SvJae/C57B6 F1 background), and mouse ESC-derived Neural Precursor Cells (NPCs)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

ESCs and NPCs are two setm cell types which rely on expression of the transcription factor Sox2. We profilled gene expression in ESCs and NPCs to correlate genome-wide Sox2 ChIP-Seq data in these cells with expression of putative targets

Publication Title

SOX2 co-occupies distal enhancer elements with distinct POU factors in ESCs and NPCs to specify cell state.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE67361
IL-17A and IL-6 -stimulated expression data from primary epithelial cell cultures derived from human trachea tissues
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

RNAs were isolated from primary cultures after 24 hour treatment with IL-17A or IL-6 (10 ng/ml) in primary human TBE cells.

Publication Title

IL-17 markedly up-regulates beta-defensin-2 expression in human airway epithelium via JAK and NF-kappaB signaling pathways.

Sample Metadata Fields

Specimen part

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accession-icon GSE52998
Adenovirus promotes host cell anabolic glucose metabolism via MYC activation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Adenovirus infection leads to increased glycolytic metabolism in host cells. Expression of a single gene product encoded within the E4 early transcription region, E4ORF1, is sufficient to promote increased glycolytic flux in cultured epithelial cells.

Publication Title

Adenovirus E4ORF1-induced MYC activation promotes host cell anabolic glucose metabolism and virus replication.

Sample Metadata Fields

Cell line

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accession-icon SRP080956
The spectrum and regulatory landscapes of intestinal innate lymphoid cells are shaped by the microbiome (single cells)
  • organism-icon Mus musculus
  • sample-icon 46 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Innate lymphoid cells (ILCs) are critical modulators of mucosal immunity, inflammation, and tissue homeostasis, but their full spectrum of cellular states and regulatory landscapes remain elusive. Here, we use a combination of genome-wide RNA-seq, ChIP-seq and ATAC-seq to compare the transcriptional and epigenetic identity of small intestinal ILCs, identifying thousands of distinct gene profiles and regulatory elements. Single-cell RNA-seq, cytometry, and imaging analyses reveal functional compartmentalization of cytokine expression and metabolic activity within the three classical ILC subtypes, and highlight transcriptional states beyond the current canonical classification. In addition, using antibiotic intervention and germ-free mice, we characterize the effect of the microbiome on the ILC regulatory landscape, and determine the response of ILCs to microbial colonization at the single-cell level. Together, our work characterizes the spectrum of transcriptional identities of small intestinal ILCs and describes how ILCs differentially integrate signals from the microbial microenvironment to generate phenotypic and functional plasticity. Overall design: ILC1(CD45+CD3-CD19-GR1-B220-CD127+ROR?t-NkP46+), ILC2(CD45+CD3-CD19-GR1-B220-CD127+ROR?t-KLRG1+) and ILC3(CD45+CD3-CD19-GR1-B220-CD127+ROR?t+) were isolated from small intestine lamina propria of WT C57Bl/6 ROR?t-GFP mice, or antibiotics treated mice (vancomycin, ampicillin,kanamycin, and metronidazole)

Publication Title

The Spectrum and Regulatory Landscape of Intestinal Innate Lymphoid Cells Are Shaped by the Microbiome.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE45291
Inhibition of Lymphotoxin-LIGHT Signaling Reduces the Interferon Signature in Rheumatoid Arthritis Patients
  • organism-icon Homo sapiens
  • sample-icon 519 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Whole blood expression was profiled in Rheumatoid Arthiritis and SLE (Systemic LUPUS Erythomatosus) patients.

Publication Title

Lymphotoxin-LIGHT pathway regulates the interferon signature in rheumatoid arthritis.

Sample Metadata Fields

Specimen part, Disease, Time

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accession-icon SRP014791
H2AZ extended acidic patch is necessary for formation specialized chromatin states in ESCs [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The H2A variant H2AZ is essential for embryonic development and for proper execution of developmental gene expression programs in embryonic stem cells (ESCs). Divergent regions in H2AZ are likely key for its functional specialization, but we know little about how these differences contribute to chromatin regulation. Here, we show that the extended acidic patch, specifically the three divergent residues in the C-terminal docking domain, is necessary for lineage commitment during ESC differentiation and proper execution of gene expression programs during ESC differentiation. Surprisingly, disruption of the acidic patch domain has a distinct consequence on cellular specification compared to H2AZ depletion. This is consistent with differences in gene expression profiles of H2AZ –depleted and acidic patch (AP) mutant ESCs during early lineage commitment. Interestingly, the distinct consequence of AP mutant expression on gene regulation is coincidence with an altered destabilized chromatin state and high chromatin mobility dependent on active transcription. Collectively, our data shows that the divergent residues within the acidic patch domain are key structural determinants of H2AZ function and links chromatin structure and dynamics with gene regulation and cell fate specification. Overall design: H2AZ extended acidic patch was mutated, or H2AZ was KD in mouse embryonic stem cells and RNA-Seq analysis was performed on the resulting cultures. Characterization of H2AZ-WT and -AP3-mutant binding specificities were performed by ChIP-Seq.

Publication Title

H2A.Z acidic patch couples chromatin dynamics to regulation of gene expression programs during ESC differentiation.

Sample Metadata Fields

Specimen part, Cell line, Subject, Time

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accession-icon GSE60038
Genome-wide analysis of high glucose and DZNep (EZH2 inhibitor) induced gene expression by mouse podocytes
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Analysis of DZNep-induced gene expression changes in cultured podocytes. The hypothesis tested in the present study was that DZnep ultimately augments Txnip expression, increasing oxidative stress in podocytes. These results provide important information on the response of podocytes to histone methyltransferase inhibition and a possible mechanism for DZNep action in podocytes.

Publication Title

The Histone Methyltransferase Enzyme Enhancer of Zeste Homolog 2 Protects against Podocyte Oxidative Stress and Renal Injury in Diabetes.

Sample Metadata Fields

Specimen part

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accession-icon SRP113200
RNA-seq data of intestinal epithelial cells and lamina propria dendritic cells
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

We report that Klebsiella pneumoniae promote Th1 cell induction in colon. To examine the influence of Klebsiella on colonic epithelial cells (ECs) and lamina propria CD11c+ dendritic cells (DCs), we performed RNA seq on them. Germ free mice were orally inoculated with Kp-2H7 or BAA-2552 and total RNA was isolated from colonic ECs and DCs 1 week after inoculation. Furthermore, we examined the involvement of TLRs in induction of Th1 cells using Myd88 KO, Trif KO, Myd88/Trif DKO mice. These deficient germ free mice were orally inoculated with Kp-2H7 and total RNA was isolated from colonic ECs 3 weeks after inoculation. Overall design: The gene expression of colonic ECs and DCs isolated from germ free mice, and GF mice inoculated with Kp-2H7 or BAA-2552, and colonic ECs isolated from GF Myd88 KO, Trif KO or Myd88/Trif DKO mice inoculated with Kp-2H7.

Publication Title

Ectopic colonization of oral bacteria in the intestine drives T<sub>H</sub>1 cell induction and inflammation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP072732
Microglia development follows a stepwise program to regulate brain homeostasis - RNA seq
  • organism-icon Mus musculus
  • sample-icon 83 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Microglia play important roles in life-long brain maintenance and in pathology, but are also crucial in the developing central nervous system; yet their regulatory dynamics during development have not been fully elucidated. Genome-wide chromatin and expression profiling coupled with single-cell transcriptomic analysis throughout development reveal that microglia undergo three temporal developmental stages in synchrony with the brain: early, pre-, and adult microglia, which are under the control of distinct regulatory circuits. Knockout of the transcription factor MafB caused disruption of homeostasis in adulthood and increased inflammation. Environmental perturbations, such as the microbiome or prenatal immune activation, led to dysregulation of the developmental program, particularly in terms of inflammation. Together, our work identifies a stepwise developmental program of microglia integrating immune response pathways that may be associated with several neurodevelopmental disorders. Overall design: Yolk sac progenitors (CD45+CD11B+CX3CR1-GFP+), microglia from early brain (CD45+CD11B+CX3CR1-GFP+), and microglia from later stages (CD45intCD11BintCX3CR1-GFP+) were isolated from CX3CR1+ C57BL/6J mice or microglia from perturbation models (CD45intCD11Bint) from mice of C57BL/6J background

Publication Title

Microglia development follows a stepwise program to regulate brain homeostasis.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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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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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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