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accession-icon SRP017869
Quantitative Different Analysis of antimicrobial peptide LL37 expressed in E.coli Top 10 under aerobic and anaerobic condition.
  • organism-icon Escherichia coli
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We reported the transcriptional profiles of E.coli expressing antimicrobial peptide LL37 under stress response condition. Overall design: 4 samples, two groups, one group is under aerobic condition, the other group is under anaerobic condition. One of samples is E.coli which expressed LL37 as induction in each group, another sample is E.coli with no LL37 expression in vivo as control in each group.

Publication Title

Effect of intracellular expression of antimicrobial peptide LL-37 on growth of escherichia coli strain TOP10 under aerobic and anaerobic conditions.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE41362
Gene expression by myriocin treatment
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Studies of aging and longevity are revealing how diseases that shorten life can be controlled to improve the quality of life and lifespan itself. Two strategies under intense study to accomplish this goal are rapamycin treatment and calorie restriction. New strategies are being discovered including one that uses low-dose myriocin treatment. Myriocin inhibits the first enzyme in sphingolipid synthesis in all eukaryotes and we showed recently that low-dose myriocin treatment increases yeast lifespan at least in part by down-regulating the sphingolipid-controlled Pkh1/2-Sch9 (ortholog of mammalian S6 kinase) signaling pathway.

Publication Title

Reducing sphingolipid synthesis orchestrates global changes to extend yeast lifespan.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE57538
MYC is an early response regulator of human adipogenesis in adipose stem cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

MYC is induced early in human adipose stem cells in response to a standard MDIR adipogenic cocktail. The objective of this experiment was to identify key gene networks impacted by MYC loss-of-function in a mixed donor pool of human derived adipose stem cells.

Publication Title

MYC is an early response regulator of human adipogenesis in adipose stem cells.

Sample Metadata Fields

Sex, Race

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accession-icon SRP163086
TL1A is a central regulator of group 3 innate lymphoid cell function in colitis
  • organism-icon Mus musculus
  • sample-icon 37 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Inflammatory bowel disease (IBD) results from a dysregulated interaction between the microbiota and a genetically susceptible host. Genetic studies have linked TNFSF15 polymorphisms and its protein TNF-like ligand 1A (TL1A) with IBD, but the functional role of TL1A in linking tissue homeostasis and intestinal inflammation is not known. Here, using cell-specific genetic deletion models, we report an essential role for CX3CR1+ mononuclear phagocyte (MNP)-derived TL1A, which is induced by adherent IBD-associated microbiota, in regulating group 3 innate lymphoid cell (ILC3) production of IL-22 and mucosal healing in acute colitis. However, in contrast to this protective role in acute colitis, TL1A-dependent expression of OX40L in MHCII+ ILC3 during colitis leads to co-stimulation of antigen-specific T cells and is required for chronic T cell colitis. These results identify a new role for ILC3 in regulating intestinal T cells and reveal a central role for TL1A in regulating ILC3 barrier immunity during colitis. Overall design: RNA from media- or TL1A-stimulated sorted Lin-CD127+IL23R-GFP+ ILC3s from IL23R-GFP/WT mice

Publication Title

Microbiota-Induced TNF-like Ligand 1A Drives Group 3 Innate Lymphoid Cell-Mediated Barrier Protection and Intestinal T Cell Activation during Colitis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE39886
Selective inhibition of CD4+ T-cell cytokine production and autoimmunity by BET protein and c-Myc inhibitors
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Bromodomain-containing proteins bind acetylated lysine residues on histone tails and are involved in the recruitment of additional factors that mediate histone modifications and enable transcription. A compound, I-BET-762, that inhibits binding of an acetylated histone peptide to BRD4 and other proteins of the BET (bromodomain and extra-terminal domain) family, was previously shown to suppress the production of pro-inflammatory proteins by macrophages and block acute inflammation in mice. Here we investigate the effect of I-BET-762 on T cell function. We show that treatment of nave CD4+ T cells with I-BET-762 during early differentiation modulates subsequent cytokine production, and inhibits the ability of Th1-skewed cells to induce autoimmune pathogenesis in a model of experimental autoimmune encephalomyelitis (EAE) in vivo. The suppressive effects of I-BET-762 on T-cell mediated inflammation were not due to inhibition of expression of the pro-inflammatory cytokines, IFN-. or IL-17, but correlated with the ability to suppress GM-CSF production from CNS-infiltrating T cells, resulting in decreased recruitment of macrophages and granulocytes. The effects of I-BET-762 were distinct from those of the fumarate ester, dimethyl fumarate (DMF), a candidate drug for treatment of multiple sclerosis (MS). Our data suggest that I-BET and DMF could have complementary roles in the treatment of MS, and provide a strong rationale for inhibitors of BET-family proteins in the treatment of autoimmune diseases, based on their dual ability to suppress granulocyte and macrophage recruitment by T cells as well as production of pro-inflammatory proteins by macrophages.

Publication Title

Selective inhibition of CD4+ T-cell cytokine production and autoimmunity by BET protein and c-Myc inhibitors.

Sample Metadata Fields

Specimen part

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accession-icon GSE67076
Array of CCR6+ ILC3 from the mesenteric lymph node of nave C57BL/6 mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

CCR6+ innate lymphoid cells were sorted from the mesenteric lymph node of nave C57BL/6 mice

Publication Title

Immune tolerance. Group 3 innate lymphoid cells mediate intestinal selection of commensal bacteria-specific CD4⁺ T cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE14810
Microarray data from murine C3H/10T1/2 and 3T3 L1 adipocytes
  • organism-icon Mus musculus
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Growing evidence indicates that PPAR agonists, such as rosiglitazone (RSG,), induce adipose mitochondrial biogenesis. Using microarrays, we systematically analyzed nucleus-encoded mitochondrial gene expression in two common murine adipocyte models, 3T3 L1 and C3H/10T1/2 adipocytes, and aimed to further establish the direct role of RSG, and capture the temporal changes in mitochondrial gene transcription during this process.

Publication Title

Rosiglitazone Induces Mitochondrial Biogenesis in Differentiated Murine 3T3-L1 and C3H/10T1/2 Adipocytes.

Sample Metadata Fields

Specimen part

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accession-icon GSE99967
Identification of a neutrophil-related gene expression signature that distinguishes between adult patients with and without nephritis in active systemic lupus erythematosus
  • organism-icon Homo sapiens
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Both a lack of biomarkers and relatively ineffective treatments constitute impediments to management of lupus nephritis (LN). Here we used gene expression microarrays to contrast the transcriptomic profiles of active SLE patients with and without LN to identify potential biomarkers for LN. RNA isolated from whole peripheral blood of active SLE patients was used for transcriptomic profiling and the data analyzed by linear modeling, with corrections for multiple testing. Results were validated in a second cohort of SLE patients, using NanoString technology. The majority of genes demonstrating altered mRNA abundance between patients with and without LN were neutrophil-related. Findings in the validation cohort confirmed this observation and showed that the levels of gene expression in renal remission were similar to active patients without LN. In secondary analyses, gene expression correlated with disease activity, hematuria and proteinuria, but not renal biopsy changes. As expression levels of the individual genes correlated strongly with each other, a composite neutrophil score was generated by summing all levels before examining additional correlations. There was a modest correlation between the neutrophil score and the blood neutrophil count, which was largely driven by the dose of steroids and not the proportion of low density and/or activated neutrophils. Analysis of longitudinal data revealed no correlation between baseline neutrophil score or changes over the first year of follow-up with subsequent renal flare or treatment outcomes, respectively. The findings argue that although the neutrophil score is associated with LN, its clinical utility as a biomarker may be limited.

Publication Title

Identification of a neutrophil-related gene expression signature that is enriched in adult systemic lupus erythematosus patients with active nephritis: Clinical/pathologic associations and etiologic mechanisms.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage

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accession-icon GSE67766
Cancer Cells Hijack PRC2 to Modify Multiple Cytokine Pathways
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Cancer Cells Hijack PRC2 to Modify Multiple Cytokine Pathways.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE67628
The effect of SUZ12 knockdown on the responsivness of IFNg Stimulated Genes
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina HumanWG-6 v3.0 expression beadchip

Description

We studied the effect of knowking down SUZ12 +/- knowckdown of BRM on the responsivness of IFNg stimulated genes. Cells were transfected with siSZU12+/-siBRM or control siRNA+/-siBRM. Cells were then left untreated or exposed to IFNg for 6 hours.

Publication Title

Cancer Cells Hijack PRC2 to Modify Multiple Cytokine Pathways.

Sample Metadata Fields

Cell line

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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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