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accession-icon SRP076404
Expression profiles in Caenorhabditis elegans mutants lacking an intestinally expressed microRNA mir-60 that promote adaptive response against chronic oxidative stress
  • organism-icon Caenorhabditis elegans
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Recent revelations into microRNA function suggest that microRNAs serve as a key player in a robust adaptive response against stress in animals through their fine-tuning capability in gene expression. However, it remains largely unclear how a microRNA-modulated downstream mechanism contributes to the process of homeostatic adaptation. Here we show that loss of an intestinally expressed microRNA gene mir-60 in the nematode C. elegans promotes adaptive response against oxidative stress; animals lacking mir-60 dramatically extend lifespan under a mild and long-term oxidative stress condition, while they do not increase resistance against a strong and transient oxidative stress exposure. We found that canonical stress responsive factors, such as DAF-16/FOXO, are dispensable for mir-60 loss to enhance oxidative stress resistance. Gene expression profiles revealed that genes encoding lysosomal proteases and those involved in the xenobiotic metabolism and pathogen defense response are up-regulated by the mir-60 loss. Detailed genetic studies and computational microRNA target prediction suggest that endocytosis components and a bZip transcription factor gene zip-10, which functions in innate immune response, are directly modulated by miR-60 in the intestine. Our findings suggest that the mir-60 loss facilitates adaptive response against chronic oxidative stress by ensuring the maintenance of cellular homeostasis. Overall design: To identify genes that respond to the mir-60 loss, RNA expression profiles were examined between the mir-60 loss mutant (mir-60(n4947)) and its control animals using the high-throughput sequencing technology. In this study, we used spe-9(hc88), a temperature-sensitive sterile strain, which has been shown in previous studies to have a lifespan similar to wild-type and widely used in gene expression studies to reduce the effect of RNA contamination from younger progenies. Both spe-9 single and mir-60;spe-9 double mutant animals were cultured at a restrictive temperature 23.5 °C, and treated with paraquat 5 mM during adulthood for chronic oxidative stress. Total RNAs were purified at the following time points: Day 0 young adult for both spe-9 and mir-60;spe-9 (just before paraquat exposure); Day 7 for both spe-9 and mir-60;spe-9 (50% survival time for spe-9); Day 10 for mir-60;spe-9 (50% survival time for mir-60;spe-9). For Day 0 controls, total RNAs were isolated twice independently for biological replicates. cDNA libraries were made for these 7 samples with indexed adapters using TruSeq Stranded mRNA Sample Prep Kit (Illumina), and sequenced on 2 lanes of flow cells on the HiSeq 2000/2500 platform, eventually providing 14 sequencing samples.

Publication Title

An intestinal microRNA modulates the homeostatic adaptation to chronic oxidative stress in <i>C. elegans</i>.

Sample Metadata Fields

Specimen part, Treatment, Subject, Time

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accession-icon GSE137192
Effect of total-body Irradiation on gene expression in mouse whole blood
  • organism-icon Mus musculus
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

For victims of radiological accidents, rapid dose estimation and damage prediction are essential. Administering the gold-standard biodosimetry chromosome aberration assay requires highly skilled individuals and several days of labor; consequently, rapid turnaround is an important concern. Identification of new dose estimation markers and damage-predicting in vivo molecules to replace the chromosome aberration assay is crucial to improving the delivery time of medical treatment. Here, we investigated the applicability of mRNA levels using a mouse model. Female C57BL/6J mice were X-ray irradiated at various doses, and a DNA microarray was then performed to identify differentially expressed mRNAs in whole blood. The microarray analysis identified 14 radioresponsive mRNAs with more than fourfold differences by pattern matching in the expression at 24 h postirradiation. In particular, mRNA expression of Slfn4, Itgb5, Smim3, Tmem40, Litaf, Gp1bb and Cxx1c was significantly increased in a radiation-dose-dependent manner, as validated by reverse transcription quantitative polymerase chain reaction. We also performed an analysis using the cBioPortal for Cancer Genomics and found that the overall survival of ovarian adenocarcinoma patients with alterations in Smim3 and that of thymoma patients with alterations in Cxx1c had a worse prognosis than patients without these alterations. These findings suggest that the expression of several genes in whole blood was a sensitive and specific biomarker of radiation exposure and can be used as a rapid and reliable prospective molecular biomarker in radiological emergencies.

Publication Title

Identification of Radiation-Dose-Dependent Expressive Genes in Individuals Exposed to External Ionizing Radiation.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE25471
Expression profile in HEK293T cells transfected with control or ZAPS expression vector
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of HEK293T cells overexpressing ZAPS (zinc finger antiviral protein, short form; NP_078901), which is a member of the PARP (poly (ADP-ribose) polymerase)-superfamily. Results of gene profiles provide insight into the role of ZAPS in innate immunity.

Publication Title

ZAPS is a potent stimulator of signaling mediated by the RNA helicase RIG-I during antiviral responses.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE43221
Transcript levels in CCE WT and RARgamma knockout murine embryonic stem cells treated with either all-trans retinoic acid (8 and 24 hr) or with vehicle control
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Retinoic acid receptors (RARs) , , and heterodimerize with Retinoid X receptors (RXR) , , and and bind the cis-acting response elements known as RAREs to execute the biological functions of retinoic acid during mammalian development. RAR mediates the anti-proliferative and apoptotic effects of retinoids in certain tissues and cancer cells, such as melanoma and neuroblastoma cells. Furthermore, ablation of RAR enhanced the tumor incidence of Ras transformed keratinocytes and was associated with resistance to retinoid mediated growth arrest and apoptosis.

Publication Title

RARγ is essential for retinoic acid induced chromatin remodeling and transcriptional activation in embryonic stem cells.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE10953
Cellular pathways involved in the adaptation and progression of motor neuron injury in the mouse model of familial ALS
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Microarray analysis has been applied to the study of ALS in order to investigate gene expression in whole spinal cord homogenates of SOD1 G93A mice and human ALS cases, although the massive presence of glial cells and inflammatory factors has made it difficult to define which gene expression changes were motor neuron specific. Recently, laser capture microdissection (LCM), combined with microarray analysis, has allowed the identification of motor neuron specific changes in gene expression in human ALS cases.

Publication Title

Microarray analysis of the cellular pathways involved in the adaptation to and progression of motor neuron injury in the SOD1 G93A mouse model of familial ALS.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE51427
Eye-Specific Gene Expression following Embryonic Ethanol Exposure in Zebrafish: Roles for Heat Shock Factor 1
  • organism-icon Danio rerio
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Ethanol is a well-known teratogen. While this teratogenic potential is well-characterized clinically, the mechanisms through which ethanol exposure results in developmental defects remain unclear. Here we use the zebrafish model to elucidate eye-specific mechanisms that may underlie ethanol-mediated microphthalmia (reduced eye size), using time-series microarray analysis of gene expression of eye tissues of embryos exposed to 1.5% ethanol vs. untreated embryos. We identified 62 genes differentially expressed in ethanol-treated as compared to control zebrafish eyes from all sampling times over the period of retinal neurogenesis (24-48 hours post-fertilization). Application of the EDGE (extraction of differential gene expression) algorithm identified over 3000 genes differentially expressed over developmental time in ethanol-treated embryo eyes as compared to untreated embryo eyes. These lists included several genes indicating a mis-regulated cellular stress response (heat shock response) due to ethanol exposure. Combined treatment with sub-threshold levels of ethanol and a morpholino (MO) targeting heat shock factor 1 (hsf-1) mRNA resulted in a microphthalmic phenotype, suggesting convergent molecular pathways. Manipulation of the heat shock response by thermal preconditioning partially prevented ethanol-mediated microphthalmia while maintaining Hsf-1 expression. Together these data are consistent with roles for reduced Hsf-1 in mediating microphthalmic effects of embryonic ethanol exposure in zebrafish.

Publication Title

Eye-specific gene expression following embryonic ethanol exposure in zebrafish: roles for heat shock factor 1.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP094591
mRNA-seq in Drosophila larval fat body
  • organism-icon Drosophila melanogaster
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We performed mRNA-seq from hand-dissected fat body tissue from 68hr (after egg laying, AEL) and 92hr AEL Drosophila melanogaster larvae. Fat body was dissected from wild-type (OrR) males and testes were removed. We examined gene expression genome-wide with particular focus on genes in the underreplicated regions in the fat body. Overall design: Sequencing of poly-A selected RNA from 68hr AEL and 92hr AEL wild-type (OrR) Drosophila melanogaster male larvae. Sequences analyzed by Illumina sequencing. Two biological replicates are included for each developmental sample.

Publication Title

Dynamic changes in ORC localization and replication fork progression during tissue differentiation.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon SRP006898
Expression profile of 16C ovarian follicle cells
  • organism-icon Drosophila melanogaster
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

We use DSN normalized RNA-seq to transcriptionally profile FACS sorted 16C ovarian follicle cells. These data provide insights into the developmental control of gene expression programmed gene amplificaton. Overall design: Follicle cells were isolated from whole ovaries by trypsinization and filtering and stained with Hoescht. 16C follicle cells were isolated by FACS sorting based on DNA content (Hoescht). RNA was extracted with TRIzol reagent and 100ng of total RNA and used to generate a total library. This library was then subjected to DSN normalization prior to Illumina based sequencing.

Publication Title

Integrative analysis of gene amplification in Drosophila follicle cells: parameters of origin activation and repression.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE52452
Gene expression data from MGHU3 bladder cancer cells (FGFR3-Y375C) treated with TAK1 siRNA and/or PD173074
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The NFB transcription factor is constitutively active in a number of hematologic and solid tumors, and many signaling pathways implicated in cancer are likely connected to NFB activation. A critical mediator of NFB activity is TGF-activated kinase 1 (TAK1). Here, we identify TAK1 as a novel interacting protein and direct target of fibroblast growth factor receptor 3 (FGFR3) tyrosine kinase activity.

Publication Title

Fibroblast growth factor receptor 3 interacts with and activates TGFβ-activated kinase 1 tyrosine phosphorylation and NFκB signaling in multiple myeloma and bladder cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE44211
Gene expression in Escherichia coli treated with human PGRP, gentamicin, and CCCP
  • organism-icon Escherichia coli
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix E. coli Genome 2.0 Array (ecoli2)

Description

Human Peptidoglycan Recognition Proteins (PGRPs) kill bacteria, likely by over-activating stress responses in bacteria. To gain insight into the mechanism of PGRP killing of Escherichia coli and bacterial defense against PGRP killing, gene expression in E. coli treated with a control protein (bovine serum albumin, BSA), human recombinant PGRP (PGLYRP4), gentamicin (aminoglycoside antibiotic), and CCCP (membrane potential decoupler) were compared. Each treatment induced unique and somewhat overlapping pattern of gene expression. PGRP highly increased expression of genes for oxidative and disulfide stress, detoxification and efflux of Cu, As, and Zn, repair of damaged proteins and DNA, methionine and histidine synthesis, energy generation, and Fe-S clusters repair. PGRP also caused marked decrease in the expression of genes for Fe uptake and motility.

Publication Title

Peptidoglycan recognition proteins kill bacteria by inducing oxidative, thiol, and metal stress.

Sample Metadata Fields

Specimen part

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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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