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accession-icon GSE65166
Whole genome analysis of cells permissive for late gene expression of HPV-16
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Aim was to identify cellular factors that regulate HPV-16 late gene expression at the level of RNA processing

Publication Title

Heterogeneous Nuclear Ribonucleoprotein C Proteins Interact with the Human Papillomavirus Type 16 (HPV16) Early 3'-Untranslated Region and Alleviate Suppression of HPV16 Late L1 mRNA Splicing.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE37841
Expression data from Prkch-/-Apoe-/- mouse
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To examine function of PKCh for atherosclerosis, we compared the gene expression profiles of control Apoe-/- and Prkch-/-Apoe-/- mice by microarray analysis.

Publication Title

PKCη deficiency improves lipid metabolism and atherosclerosis in apolipoprotein E-deficient mice.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE40714
Fosb gene products contribute to excitotoxic microglial activation by regulating the expression of complement C5a receptors in microglia
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The Fosb gene encodes subunits of the activator protein-1 transcription factor complex. Two mature mRNAs, Fosb and Fosb, encoding full-length FOSB and FOSB proteins respectively, are formed by alternative splicing of Fosb mRNA. Fosb products are expressed in several brain regions. Moreover, Fosb-null mice exhibit depressive-like behaviors and adult-onset spontaneous epilepsy, demonstrating important roles in neurological and psychiatric disorders. Study of Fosb products has focused almost exclusively on neurons; their function in glial cells remains to be explored. In this study, we found that microglia express equivalent levels of Fosb and Fosb mRNAs to hippocampal neurons and, using microarray analysis, we identified six microglial genes whose expression is dependent on Fosb products. Of these genes, we focused on C5ar1 and C5ar2, which encode receptors for complement C5a. In isolated Fosb-null microglia, chemotactic responsiveness toward the truncated form of C5a was significantly lower than that in wild-type cells. Fosb-null mice were significantly resistant to kainate-induced seizures compared with wild-type mice. C5ar1 mRNA levels and C5aR1 immunoreactivity were increased in wild-type hippocampus 24 hours after kainate administration; however, such induction was significantly reduced in Fosb-null hippocampus. Furthermore, microglial activation after kainate administration was significantly diminished in Fosb-null hippocampus, as shown by significant reductions in CD68 immunoreactivity, morphological change and reduced levels of Il6 and Tnf mRNAs, although no change in the number of Iba-1-positive cells was observed. These findings demonstrate that, under excitotoxicity, Fosb products contribute to a neuroinflammatory response in the hippocampus through regulation of microglial C5ar1 and C5ar2 expression.

Publication Title

Fosb gene products contribute to excitotoxic microglial activation by regulating the expression of complement C5a receptors in microglia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37056
Expression data from fosb gene modified mouse
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To examine fosB regulation of neurogenesis, depression and epilepsy, we compared the gene expression profiles of wild type, fosBd/d and fosB-null mice by microarray analysis.

Publication Title

fosB-null mice display impaired adult hippocampal neurogenesis and spontaneous epilepsy with depressive behavior.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE35166
Regulation of inflorescence architecture by inter-tissue-layer ligand-receptor communication between endodermis and phloem
  • organism-icon Arabidopsis thaliana
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Inflorescence architecture of Arabidopsis thaliana is regulated by ER-EPFL4/6 signaling module. To analyze the genes governed by this module, the transcriptional profiles of er-2 (allelic to er-106) mutant and epfl4 epfl6 double mutant were investigeted.

Publication Title

Regulation of inflorescence architecture by intertissue layer ligand-receptor communication between endodermis and phloem.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE35011
PPARg agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPAR ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here we show that PPAR ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPAR agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a novel therapeutic pathway for the treatment of obesity and diabetes.

Publication Title

PPARγ agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein.

Sample Metadata Fields

Sex

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accession-icon GSE3595
Identification of potential KLF7 target genes in olfactory sensory neurons
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

KLF7 null mice show profound axonal growth defects in the olfactory epithelium. The goal of this study was the identification of potential KLF7 target genes in olfactory sensory neurons.

Publication Title

Identification of genes regulated by transcription factor KLF7 in differentiating olfactory sensory neurons.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE27867
Expression data from C. elegans (wild type vs. tag-24)
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

To provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa.

Publication Title

Neuronal GPCR controls innate immunity by regulating noncanonical unfolded protein response genes.

Sample Metadata Fields

Specimen part

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accession-icon GSE37305
Age and Fasting in C. elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The Sexual Dimorphism of Dietary Restriction Responsiveness in Caenorhabditis elegans.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE37303
Fasting induced changes in gene expression profiles of C. elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon

Description

Many species undergo sexual reproduction to distribute the parental genomes and increase the genomic diversity of the progeny. Among such species, sexual dimorphism is often displayed through morphology, size, behavior, and life-span, depending on the survival and reproduction strategies of the species. The nematode Caenorhabditis elegans has two sexes, hermaphrodite and male, and only the hermaphrodites, which produce both oocytes and sperm, are essential for the perpetuation of the species. In this study, we found that dietary restriction, which is the most reproducible way to retard aging in many species, extends the life-span of C. elegans hermaphrodites but not that of males. Our analysis revealed that fasting induces male-enriched genes in hermaphrodites and that the sex determination pathway affects life-span regulation, even after the completion of development, and is regulated by food availability. Furthermore, fasting activates the entire X-chromosome only in hermaphrodites. Our tiling array analysis identified a fasting-inducible, X-linked non-coding RNA for which expression positively correlated with the activation level of the X-chromosome and longevity. These links between the sex determination mechanism and dietary restriction at multiple levels may give priority to the survival of hermaphrodites during food shortages in C. elegans.

Publication Title

The Sexual Dimorphism of Dietary Restriction Responsiveness in Caenorhabditis elegans.

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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