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accession-icon GSE31434
Expression data from HeLa cells transfected with SLC44A5
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We identified SLC44A5 as a gene associated with birth weight in cattle based on genome wide association studies.

Publication Title

The molecular effects of a polymorphism in the 5'UTR of solute carrier family 44, member 5 that is associated with birth weight in Holsteins.

Sample Metadata Fields

Cell line

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accession-icon GSE67272
Nitric oxide signaling and its role in oxidative stress response in Schizosaccharomyces pombe
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

In examining NO signaling in the fission yeast Schizosaccharomyces pombe, we found that the putative NO dioxygenase SPAC869.02c (named Yhb1) and the S-nitrosoglutathione reductase Fmd2 cooperatively reduced intracellular NO levels as NO-detoxification enzymes. Although both protein levels were increased with exogenous NO, their expression patterns were different during growth phases. While expression of Yhb1 in the log phase was abrogated by treatment with an NO synthase inhibitor, induction of Fmd2 in the stationary phase was correlated with elevated mitochondrial respiratory chain (MRC) activity and reactive oxygen species (ROS) generation. Moreover, NO was localized in the mitochondria specifically in the stationary phase, suggesting that there are at least two distinctive types of NO signaling in S. pombe cells. For mitochondrial NO signaling, pretreatment with an NO donor effectively rescued the cell viability by repressing generation of ROS under oxidative stress. DNA microarray analysis revealed that exogenous NO contributes to tolerance to hydrogen peroxide (H2O2) stress by (i) inhibition of Fe3+ to Fe2+conversion, (ii) upregulation of the H2O2-detoxifying enzymes, and (iii) downregulation of the MRC genes. Therefore, NO is suggested to play a pivotal role in the negative feedback system to regulate ROS levels under oxidative stress in S. pombe cells.

Publication Title

Nitric oxide signaling and its role in oxidative stress response in Schizosaccharomyces pombe.

Sample Metadata Fields

Treatment

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accession-icon GSE22434
Expression data from Evi1-transduced primary bone marrow cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Evi1 is essential for proliferation of hematopoietic stem cells and implicated in the development of myeloid disorders. Particularly, high Evi1 expression defines one of the largest clusters in acute myeloid leukemia and is significantly associated with extremely poor prognosis. Improvement of the therapeutic outcome of leukemia with activated Evi1 is one of the most challenging issues. However, mechanistic basis of Evi1-mediated leukemogenesis has not been fully elucidated. Here we show that Evi1 directly represses PTEN transcription in the murine bone marrow, which leads to activation of AKT/mTOR signaling. In a murine bone marrow transplantation model, Evi1 leukemia showed remarkable sensitivity to an mTOR inihibitor rapamycin. Furthermore, we found that Evi1 binds to several polycomb group proteins and recruits polycomb repressive complexes for PTEN downregulation, which reveals a novel epigenetic mechanism of AKT/mTOR activation in leukemia. Expression analyses and chromatin immunoprecipitation assays using human samples indicate that our findings in mice models are recapitulated in human leukemic cells. Dependence of Evi1-expressing leukemic cells on AKT/mTOR signaling provides the first example of targeted therapeutic modalities that suppress the leukemogenic activity of Evi1. The PTEN/AKT/mTOR signaling pathway and the Evi1-polycomb interaction can be promising therapeutic targets for leukemia with activated Evi1.

Publication Title

Evi1 represses PTEN expression and activates PI3K/AKT/mTOR via interactions with polycomb proteins.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE43382
Gene-expression change along with differentiation stage from human iPS cells to astrocytes
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

gene-expression change along with differentiation stage from human iPS cells to astrocytes is unkown.

Publication Title

Modeling Alzheimer's disease with iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness.

Sample Metadata Fields

Specimen part

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accession-icon GSE43326
Gene expression data from iPSC-derived neural cells, comparison between APP wild and E693delta mutation
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Oligomeric forms of amyloid-beta peptide (Abeta) are presumed to play a pivotal role in the pathogenesis of Alzheimers disease (AD). However, it is still unclear how Abeta oligomers contribute to AD pathogenesis in patient neural cells. We generated induced pluripotent stem cells (iPSCs) from a familial AD patient and differentiated them into neural cells. Abeta oligomers were accumulated in neural cells of AD bearing amyloid precursor protein (APP)-E693delta mutation.

Publication Title

Modeling Alzheimer's disease with iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness.

Sample Metadata Fields

Specimen part

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accession-icon GSE41358
Expression data from mouse preimplantation cloned embryos
  • organism-icon Mus musculus
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transcriptiome analysis is an excellent approach to understand the mechanism underlying nuclear reprogramming in somatic-cell-cloned embryos. Analysis of the transcriptomic data from the oocyte to blastocyst stage revealed that specific genes were inappropriately reprogrammed at each stage. Sertoli cell-cloned embryos appear to develop normally because the progression of incorrect reprogramming is concealed throughout development.

Publication Title

The transcriptomic architecture of mouse Sertoli cell clone embryos reveals temporal–spatial-specific reprogramming.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE45826
Expression data from sorted control and Pygo2-null mouse mammary stem/basal cells
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Skin-mammary specific knockout (SSKO) of Pygo2 (K14-cre; Pygo2 flox/-) , a WNT signaling co-activator, results in defective mouse mammary gland development.

Publication Title

Chromatin effector Pygo2 mediates Wnt-notch crosstalk to suppress luminal/alveolar potential of mammary stem and basal cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP096355
Transcriptome analysis of p16/p21-dependent monocytic myeloid-derived suppressor cells accumulation.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

p16 and p21 act as tumor suppressors through induction of cellular senescence. However, senescence-independent roles of these CDK inhibitors are not known. To identify the mechanism responsible for the failure of Mo-MDSCs (monocytic myeloid-derived suppressor cells) infiltration into tumor allografts in p16/p21-double knockout (DKO) mice, we searched for chemokine receptors that were highly expressed in Mo- but not PMN-MDSCs (polymorphonuclear myeloid-derived suppressor cells) and were downregulated in p16/p21-DKO as compared to WT Mo-MDSCs. Ccr2, Ccr5, and Cx3cr1 were identified by RNA-seq analysis. Overall design: RNA sequencing was performed using PMN-MDSCs derived from wild-type mice (WT), Mo-MDSCs derived from WT mice and Mo-MDSCs derived from p16/p21 DKO mice in triplicates, respectively.

Publication Title

p16<sup>Ink4a</sup> and p21<sup>Cip1/Waf1</sup> promote tumour growth by enhancing myeloid-derived suppressor cells chemotaxis.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE6185
Stress response of Saccharomyces cerevisiae to exposure to natural product pyocyanin.
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

Pyocyanin has been shown to engage in redox transfer of electrons from NADPH to oxygen to generate superoxide radicals. Transcriptional response to oxygen stress has been characterized in yeast and should be observable upon exposure to pyocyanin if this is the true mode of action.

Publication Title

Pyocyanin isolated from a marine microbial population: synergistic production between two distinct bacterial species and mode of action.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP016946
Transcriptome analysis in mouse early round spermatids deficient in pachytene piRNAs (Miwi+/- and -/-)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

In animal germline cells, Piwi-interacting RNAs (piRNAs) silence retrotransposons through post-transcriptional and transcriptional mechanisms. However, little is known, especially in mammals, about the functions of piRNAs beyond retrotransposon suppression1-5. In mammalian spermatocytes, piRNAs are known to be abundantly expressed6-10. Here, we show that a subset of coding and noncoding RNAs in mouse spermatocytes is degraded by the piRNA pathway. By analyzing the germline trasnscriptome of mice deficient in piRNA biogenesis, we identify hundreds of mRNAs as direct targets of piRNAs. Remarkably, the 3'' untranslated region (UTR) of the mRNAs up-regulated in the piRNA pathway mutants are highly enriched with retrotransposon sequenes, implying that these sequences serve as regulatory elements for piRNA-mediated regulation. Furthermore, deficiencies of piRNAs derived from pseudogenes result in increased mRNA levels of their cognate genes, indicating that pseudogenes regulate their functional cognates via piRNAs. Moreover, we identify a large population of testis-enriched long intergenic noncoding RNAs (lincRNAs), some of which are also degraded by the piRNA pathway. Collectively, our results reveal that the piRNA pathway regulates the expression of both mRNAs and lincRNAs in addition to retrotransposon RNAs during meiosis and the key role of retrotransposons and pseudogenes, two major types of genomic sequences, in this regulation by acting as piRNA sources and/or regulatory elements in target RNAs. Overall design: Early round spermatid mRNA profiles of Miwi+/- and -/- were analyzed by deep sequencing, in triplicate, using Illumina HiSeq.

Publication Title

Retrotransposons and pseudogenes regulate mRNAs and lncRNAs via the piRNA pathway in the germline.

Sample Metadata Fields

Specimen part, Subject

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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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