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accession-icon GSE45577
Profiling of glycerol- and CTX-induced models of muscle regeneration in mice
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Utilizing glycerol and cardiotoxin (CTX) injections in the tibialis anterior muscles of M. musculus provides models of skeletal muscle damages followed by skeletal muscle regeneration. In particular, glycerol-induced muscle regeneration is known to be associated with ectopic adipogenesis. We characterized genome-wide expression profiles of tibialis anterior muscles from wild-type mice injured by either glycerol or CTX injection. Our goal was to detect gene expression changes during the time course of glycerol-induced and CTX-induced muscle regeneration models, that can lead to ectopic adipocyte accumulation.

Publication Title

Genomic profiling reveals that transient adipogenic activation is a hallmark of mouse models of skeletal muscle regeneration.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE21364
mRNA expression data from keratinocytes with disorganized lipid raft structures (by cholesterol depletion by methyl-beta-cyclodextrin)
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Lipid rafts are cholesterol-rich cell signaling platforms and their physiological role can be explored by cholesterol depletion. To dress a global picture of transcriptional changes ongoing after lipid raft disruption, we performed whole-genome expression profiling in epidermal keratinocytes, a cell type which synthesizes its cholesterol in situ.

Publication Title

Transcriptional profiling after lipid raft disruption in keratinocytes identifies critical mediators of atopic dermatitis pathways.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE13296
miR-155 KO in human dendritic cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In response to inflammatory stimulation, dendritic cells (DCs) have a remarkable pattern of differentiation (maturation) that exhibits specific mechanisms to control immunity. Here, we show that in response to Lipopolysaccharides (LPS), several microRNAs (miRNAs) are regulated in human monocyte-derived dendritic cells. Among these miRNAs, miR-155 is highly up-regulated during maturation. Using LNA silencing combined to microarray technology, we have identified the Toll-like receptor / interleukin-1 (TLR/IL-1) inflammatory pathway as a general target of miR-155. We further demonstrate that miR-155 directly controls the level of important signal transduction molecules. Our observations suggest, therefore, that in mature human DCs, miR-155 is part of a negative feedback loop, which down-modulates inflammatory cytokine production in response to microbial stimuli.

Publication Title

MicroRNA-155 modulates the interleukin-1 signaling pathway in activated human monocyte-derived dendritic cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17460
Expression data from MCF-7 cells transfected with miR-26a and treated or not with estradiol
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Altered expression of microRNAs (miRNAs), an abundant class of small non-protein-coding RNAs that mostly function as negative regulators of protein-coding gene expression, is common in cancer. Here we analyze the regulation of miRNA expression in response to estrogen, a steroid hormone that is involved in the development and progression of breast carcinomas and that is acting via the estrogen receptors (ER) transcription factors. We set out to thoroughly describe miRNA expression, by using miRNA microarrays and real time RTPCR experiments, in various breast tumor cell lines in which estrogen signaling has been induced by 17-estradiol (E2). We show that the expression of a broad set of miRNAs decreases following E2 treatment in an ER-dependent manner. We further show that enforced expression of several of the repressed miRNAs reduces E2-dependent cell growth, thus linking expression of specific miRNAs with estrogen-dependent cellular response. In addition, a transcriptome analysis revealed that the E2-repressed miR-26a and miR-181a regulate many genes associated with cell growth and proliferation, including the progesterone receptor gene, a key actor in estrogen signaling. Strikingly, miRNA expression is also regulated in breast cancers of women who had received antiestrogen neoadjuvant therapy thereby showing an estrogen-dependent in vivo regulation of miRNA expression. Overall, our data indicates that the extensive alterations in miRNA regulation upon estrogen signalling pathway plays a key role in estrogen-dependent functions and highlights the utility of considering miRNA expression in the understanding of antiestrogen resistance of breast cancer.

Publication Title

Widespread estrogen-dependent repression of micrornas involved in breast tumor cell growth.

Sample Metadata Fields

Cell line

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accession-icon GSE39042
Expression data from MDA-MB-231 cells exposed to hypoxia and/or paclitaxel or epirubicin
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hypoxia protects cancer cells from chemotherapeutic drug-induced cell death.

Publication Title

TMEM45A is essential for hypoxia-induced chemoresistance in breast and liver cancer cells.

Sample Metadata Fields

Cell line

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accession-icon GSE14000
Fine-tuning of human dendritic cells regulation revealed by translational profiling
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Dendritic cells (DCs) are the sentinels of the mammalian immune system and they undergo a complex maturation process mediated by activation upon pathogen detection. Recent studies described the analysis of activated DCs by transcriptional profiling, but translation regulation was never taken in account. Therefore, the nature of the mRNAs being translated at various stages of DC activation was determined with the help of translational profiling, which is the sucrose gradient fractionation of polysomal-bound mRNAs combined to microarrays analysis. Total and polysomal-bound mRNA populations were compared in immature (0h) and LPS-stimulated (4h and 16h) human monocyte-derived DCs with the help of Affymetrix microarrays. Biostatistical analysis indicated that 296 mRNA molecules are translationally regulated during DC-activation. The most abundant biological process among the regulated mRNAs was protein biosynthesis, indicating the existence of a negative feedback loop regulating translation. Interestingly, a cluster of 17 ribosomal proteins were part of the regulated mRNAs, indicating that translation may be fine-tuned by particular components of the translational machinery. Our observations highlight the importance of translation regulation during the immune response, and may favour the identification of novel gene clusters or protein networks relevant for immunity. Our study also provides information on the possible absence of correlation between gene expression and real protein production in DCs.

Publication Title

Ribosomal protein mRNAs are translationally-regulated during human dendritic cells activation by LPS.

Sample Metadata Fields

No sample metadata fields

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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 GSE18172
T.F. Glis3: a novel critical player in the regulation of pancreatic beta-cell development and insulin gene expression
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Glis3 mutant mice (Glis3zf/zf) die within the first week after birth due to overt diabetes, evidenced by hyperglycemia and hypoinsulinemia. Histopathological analysis showed that Glis3zf/zf mice develop a pancreatic phenotype with a dramatic loss of beta- (insulin) and delta- (somatostatin) cells contrasting a smaller relative loss of alpha- (glucagon), PP- (pancreatic polypeptide), and epsilon- (ghrelin) cells. Glis3zf/zf mice develop ductal cysts with decreased number of primary cilia, while the acini are not significantly affected. Gene expression profiling by microarray analysis demonstrated that the expression of terminal hormonal genes and several transcription factors important in endocrine development were significantly deregulated in Glis3zf/zf mice. During pancreatic development, Glis3 mRNA expression is induced during the secondary transition, a stage of cell lineage specification and extensive patterning. Changes in pancreatic development of Glis3zf/zf mice are noted during and after this stage. The population of pancreatic progenitors appears not to be greatly affected in Glis3zf/zf mice; however, the number of neurogenin 3 (Ngn3) positive, endocrine progenitors is significantly reduced. Our study indicates that Glis3 plays a key role in cell lineage specification, particularly the development of mature pancreatic beta-cells. In addition, we identified evidence that Glis3 regulates insulin gene expression through two Glis-binding sites in its proximal promoter indicating that Glis3 is a regulator of insulin gene expression.

Publication Title

Transcription factor Glis3, a novel critical player in the regulation of pancreatic beta-cell development and insulin gene expression.

Sample Metadata Fields

Specimen part

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accession-icon GSE9810
Comparison of human and mouse dendritic cell subsets by genome-wide expression profiling
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Dendritic cells (DCs) are a complex group of cells which play a critical role in vertebrate immunity. Spleen or lymph node resident DCs are subdivided into conventional DC (cDC) subsets (CD11b and CD8alpha in mouse; BDCA1 and BDCA3 in man) and plasmacytoid DCs (pDCs). It is currently unclear if these various DC populations belong to a unique hematopoietic lineage and if the subsets identified in the mouse and human systems are evolutionary homologs. To bring novel insights into these questions, we sought conserved genetic signatures for these DCs through the analysis of a compendium of genome-wide expression profiles of mouse or human leukocytes.

Publication Title

Novel insights into the relationships between dendritic cell subsets in human and mouse revealed by genome-wide expression profiling.

Sample Metadata Fields

No sample metadata fields

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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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