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accession-icon GSE47050
Expression data from S. cerevisiae following tRNA gene deletion
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

We created a comprehensive tRNA deletion library in yeast and characterized the phenotypic and further characterized the molecular changes in a subset of deletion strains

Publication Title

A comprehensive tRNA deletion library unravels the genetic architecture of the tRNA pool.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE42255
Gene expression changes in response to aging compared to heat stress, oxidative stress and ionizing radiation in Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

Gene expression changes in response to aging, hyperoxia, hydrogen peroxide, ionizing radiation, and heat stress were compared using microarrays. While aging shared features with each stress, aging was more similar to the stresses most associated with oxidative stress (hydrogen peroxide, hyperoxia, ionizing radiation) than to heat stress. Aging is associated with down-regulation of numerous mitochondrial genes, including electron-transport-chain (ETC) genes and mitochondrial metabolism genes, and a sub-set of these changes was also observed upon hydrogen peroxide stress and ionizing radiation stress. Aging shared the largest number of gene expression changes with hyperoxia. The extensive down-regulation of mitochondrial and ETC genes during aging is consistent with an aging-associated failure in mitochondrial maintenance, which may underlie the oxidative stress-like and proteotoxic stress-like responses observed during aging.

Publication Title

Gene expression changes in response to aging compared to heat stress, oxidative stress and ionizing radiation in Drosophila melanogaster.

Sample Metadata Fields

Sex, Age

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accession-icon GSE82047
A genome-wide loss-of-function screen identifies SLC26A2 as a novel mediator of TRAIL resistance
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To identify intrinsic mechanismis that mediating Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance , gene expression analysis was performed on MDA-MB-231 cell lines exposed to TRAIL, in parental (Sensitive) or treat to resistance (TTR) conditions.

Publication Title

A Genome-Wide Loss-of-Function Screen Identifies SLC26A2 as a Novel Mediator of TRAIL Resistance.

Sample Metadata Fields

Cell line

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accession-icon SRP149147
KAP1 regulates ERVs in differentiated human cells and contributes to innate immune control
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Endogenous retroviruses (ERVs) have accumulated in vertebrate genomes and contribute to the complexity of gene regulation. KAP1 represses ERVs during development by its recruitment to their repetitive sequences through KRAB-zinc finger proteins (KZNFs), but little is known about the regulation of ERVs in differentiated cells. We observed that KAP1 repression of HERVK14C was conserved in differentiated human cells and performed KAP1 knockout to obtain an overview of KAP1 function. Our results show that KAP1 represses ERVs (including HERV-T and HERV-S) and ZNFs, both of which overlap with KAP1 binding sites and H3K9me3 in multiple cell types. Furthermore, this pathway is functionally conserved in primary peripheral blood mononuclear cells. Cytosine methylation that acts on KAP1-regulated loci is necessary to prevent an interferon response, and KAP1-depletion leads to activation of some interferon-stimulated genes. Finally, loss of KAP1 leads to a decrease in H3K9me3 enrichment at ERVs and ZNFs and an RNA-sensing response mediated through MAVS signaling. These data indicate that the KAP1-KZNF pathway contributes to genome stability and innate immune control in differentiated human cells. Overall design: Dissection of which transposons and genes KAP1 regulates in differentiated human cells

Publication Title

KAP1 regulates endogenous retroviruses in adult human cells and contributes to innate immune control.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP051510
Effect of mifepristone on gene expression in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 34 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Illumina sequencing was used to assay the effect of mifepristone treatment on gene expression in adult Drosophila, including males, virgin females and mated females. Overall design: Males of strain w[1118]; p53B[6] were crossed to virgins of w[1118]; rtTA(3)E2 and progeny males and virgins were collected over 48 hours. One half of the virgins were mated to w[1118] males at ratio of 1:1 virgins to males for 4 days. Mated females were then separated from the w[1118] males. The mated females, males and virgins females were then maintained at approximately 20 flies per vial, on food with and without supplementation with 160ug/ml mifepristone for 12 days. Total fly RNA was isolated from 20 animals per sample. Three replicate samples were generated for each type of flies: males, mated females and virgin females.

Publication Title

The progesterone antagonist mifepristone/RU486 blocks the negative effect on life span caused by mating in female Drosophila.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE65200
The Six1 oncoprotein represses translation of p53 via concomitant regulation of RPL26 and microRNA-27a
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

TP53 is mutated in 50% of all cancers, and is often functionally compromised in cancers where it is not mutated. We demonstrate that the pro-tumorigenic/metastatic Six1 homeoprotein decreases p53 levels through a mechanism that does not involve the negative regulator of p53, MDM2. Instead, Six1 regulates p53 via a dual mechanism involving upregulation of microRNA-27a and downregulation of the ribosomal protein L26 (RPL26), a positive regulator of p53 translation. Mutation analysis confirms that RPL26, whose expression inversely correlates with Six1 expression in numerous tumor types, inhibits miR-27a binding to the p53 3UTR and prevents microRNA-mediated translational inhibition of p53. Thus, through simultaneous downregulation of RPL26 and upregulation of miR-27a, Six1 efficiently lowers p53 levels despite regulation of p53 at the level of the proteasome. Consequently, Six1 overexpression, which is observed in numerous tumor types, leads to dramatic resistance to nutlins, as well as other therapies targeting the p53-MDM2 interaction.

Publication Title

The Six1 oncoprotein downregulates p53 via concomitant regulation of RPL26 and microRNA-27a-3p.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE87073
Contact of myeloma cells induces a characteristic transcriptome signature in skeletal precursor cells - Implications for myeloma bone disease
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In this study we analyzed the myeloma cell contact-mediated changes on the transcriptome of skeletal precursor cells. Therefore, human mesenchymal stem cells (MSC) and osteogenic precursor cells (OPC) were co-cultured with the representative myeloma cell line INA-6 for 24 h. Afterwards, MSC and OPC were separated from INA-6 cells by fluorescence activated cell sorting. Total RNA of MSC and OPC fractions was used for whole genome array analysis.

Publication Title

Contact of myeloma cells induces a characteristic transcriptome signature in skeletal precursor cells -Implications for myeloma bone disease.

Sample Metadata Fields

Sex, Age, Specimen part, Disease stage

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accession-icon SRP070433
Quantitative Analysis of Notch mutant (Notch1&2-null, Psen1&2-null, RBPjk-null) and wild-type hair follicle transcriptomes by NGS
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The goals of this study is to test whether NICD presence protects the RBPjk-null Hair Follicles by altering gene expression via association with other DNA binding proteins at P3, just before the conversion to TSLP-producing keratin cysts. Overall design: Methods: Skin samples were embedded in OCT. Sectioned at 20µm thickness. Dehydrated in EtOH, and equilibrated to Xylene before the LCM procedure. Laser capture was performed with Arcturus Veritas. Methods: ~100 hair follicles from Notch-null, PS-null, RBPjk-null and wild-type samples were pooled into 3 biological replicates for each genotype and subjected to RNA isolation followed by RNA-Seq. Conclusions: A total of 2047 genes were differentially expressed (=1.5 fold) in three or more biological replicates of Notch mutant hair follicles compared to wild-type controls (p-value<0.05). Unsupervised hierarchical clustering analysis failed to distinguish between the mutants.

Publication Title

The Notch Intracellular Domain Has an RBPj-Independent Role during Mouse Hair Follicular Development.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP011435
High-thoughput Illumina RNA sequencing to identify downstream target genes of RABBIT EARS (RBE) in the flowers of Arabidopsis thaliana
  • organism-icon Arabidopsis thaliana
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

In order to identify putative downstream target genes of RBE, we sequenced mRNA from dexamethasone (DEX) and mock treated transgenic Arabidopsis line 35S:GR-RBE (RBE coding region fused to a glucocorticoid receptor domain driven by the constitutive 35S promoter) floral tissues. We compared the results from DEX and mock treatments and focused on the 832 genes whose expression was significantly reduced (P < 0.025) by 2-fold or more in DEX as compared to mock-treated plants. In this analysis, we identified MIR164c (EEP1) as a candidate target of RBE, which was further confirmed by other molecular and genetic analyses. Regulation of MIR164c by RBE is important for normal floral organ formation in Arabidopsis. Overall design: We used two biological replicates, each with two technical replicates for four hour DEX or mock treated floral tissues to produce 8 sequencing libraries.

Publication Title

RBE controls microRNA164 expression to effect floral organogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE41203
Transcriptional analysis of type 1 diabetes reveals an interferon signature that precedes T cell activation
  • organism-icon Mus musculus
  • sample-icon 57 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Type 1 diabetes (T1D) is an autoimmune disease triggered by T cell reactivity to protein antigens produced by the -cells. Here we present a chronological compendium of transcriptional profiles from islets of Langerhans isolated from non-obese diabetic (NOD) mice ranging from 2 wks up to diabetes and compared to controls. Parallel analysis was made of cellular components of the islets. Myeloid cells populated the islets early during development in all mouse strains. This was followed by a type I interferon signature detectable at 4-6 wks of age only in diabetes susceptible mice. Concurrently, CD4 T cells were found within islets, many in contact with intra-islet antigen presenting cells. Early cellular signs of islet reactivity were detected by six wks. By 8 wks, NOD islets contained all major leukocytes populations and an inflammatory gene signature. This work establishes the natural transcriptional signature of T1D and provides a resource for future research.

Publication Title

Defining the transcriptional and cellular landscape of type 1 diabetes in the NOD mouse.

Sample Metadata Fields

Specimen part

View Samples

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)

fund-icon Fund the CCDL

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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