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accession-icon GSE22853
Expression data from human Ea.hy926 cells in response to epoxomicin and in dependency of TCF11 presence
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Coordinated regulation of the ubiquitin-proteasome system is crucial for the cell to adjust its protein degradation capacity to changing proteolytic requirements. The transcription factor TCF11 has been identified as a regulator for 26S-proteasome formation in human cells to compensate for reduced proteolytic activity. To expand the current knowledge of other UPS-related TCF11 target genes in response to epoxomicin, we performed microarray analyses of cells exposed to epoxomicin and with or without depletion of TCF11.

Publication Title

Proteasomal degradation is transcriptionally controlled by TCF11 via an ERAD-dependent feedback loop.

Sample Metadata Fields

Specimen part

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accession-icon GSE33399
Necrotic mutants in barley cv. Steptoe
  • organism-icon Hordeum vulgare
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Barley Genome Array (barley1)

Description

FN044, FN211, FN242 and FN303 are the fast neutron generated mutants in cv. Steptoe background. These 4 mutants have lesion mimic phenotype and increase disease resistance to stem rust. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, ling zhang. The equivalent experiment is BB54 at PLEXdb.]

Publication Title

A cation/proton-exchanging protein is a candidate for the barley NecS1 gene controlling necrosis and enhanced defense response to stem rust.

Sample Metadata Fields

Specimen part

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accession-icon GSE34811
Gene expression profiling of myelin-phagocytosing macrophages
  • organism-icon Rattus norvegicus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Multiple sclerosis is a chronic, inflammatory, demyelinating disease of the central nervous system in which macrophages and microglia play a central role. During active multiple sclerosis foamy macrophages and microglia, containing degenerated myelin, are abundantly found in demyelinated areas. Recent studies have described an altered macrophage phenotype after myelin internalization. However, by which mechanisms myelin affects the phenotype of macrophages and how this phenotype can influence lesion progression is unclear.

Publication Title

Myelin-derived lipids modulate macrophage activity by liver X receptor activation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE4635
Proteomic and Genomic Profiling of Bronchial Epithelial Cells in Never and Current Smokers
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Comparison of gene and protein expression in the large airway epithelium of never and current smokers.

Publication Title

Comparison of proteomic and transcriptomic profiles in the bronchial airway epithelium of current and never smokers.

Sample Metadata Fields

Sex, Age, Specimen part, Race, Subject

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accession-icon GSE13909
Molecular signature of cell cycle exit induced in human T lymphoblasts by IL-2 withdrawal
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Molecular mechanisms of cell cycle exit are poorly understood. A group of genes required for cell cycle exit and maintenance of cell quiescence in human fibroblasts following serum deprivation has been recently identified. Studies on lymphocytes following growth factor deprivation-induced cell cycle exit have predominantly focused on the initiation of apoptosis. A set of genes involved in lymphocyte quiescence have also been identified among genes highly expressed in resting lymphocytes and down-regulated after cell activation. In our study, proliferating IL-2-dependent human T cells were forced to exit cell cycle by growth factor withdrawal, and their gene expression profiles were examined.

Publication Title

Molecular signature of cell cycle exit induced in human T lymphoblasts by IL-2 withdrawal.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP070753
Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt
  • organism-icon Caenorhabditis elegans
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Organisms respond to mitochondrial stress through the upregulation of an array of protective genes, often perpetuating an early response to metabolic dysfunction across a lifetime. We find that mitochondrial stress causes widespread changes in chromatin structure through histone H3K9 di-methylation marks traditionally associated with gene silencing. Mitochondrial stress response activation requires the di-methylation of histone H3K9 through the activity of the histone methyltransferase met-2 and the nuclear co-factor lin-65. While globally the chromatin becomes silenced by these marks, remaining portions of the chromatin open up, at which point the binding of canonical stress responsive factors such as DVE-1 occurs. Thus, a metabolic stress response is established and propagated into adulthood of animals through specific epigenetic modifications that allow for selective gene expression and lifespan extension. Overall design: comparison of gene expression changes in response to cco-1 RNAi treatment in N2, lin-65(n3441) and met-2(ok2307) populations of C. elegans L4 animals

Publication Title

Mitochondrial Stress Induces Chromatin Reorganization to Promote Longevity and UPR(mt).

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP043224
Zea mays Transcriptome or Gene expression
  • organism-icon Zea mays
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Endosperm is a product of double fertilization, and provides nutrients and signals to the embryo during seed development in flowering plants. Early stages of endosperm development are critical for the development of its storage capacity through synthesis and accumulation of starch and storage proteins. Here we report on the isolation and sequencing of mRNAs from the central portion of the starchy endosperm of Zea mays (maize) B73 at 6 days after pollination. We detected high correlation among the four biological replicates of RNAs isolated using laser-capture microdissection of the cell type. Because the assayed stage of development precedes the synthesis and accumulation of the major storage proteins and starch in the endosperm, our dataset likely include mRNAs for genes that are involved in control and establishment of these developmental programs. Overall design: Four replicates of mRNAs from the central portion of starchy endopserm were isolated using laser-capture microdissection and sequenced using the Illumina GAIIx platform.

Publication Title

RNA-Seq analysis of laser-capture microdissected cells of the developing central starchy endosperm of maize.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon GSE80000
Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.

Sample Metadata Fields

Sex

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accession-icon GSE79999
Adam17-Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling (macrophage)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Gene expression analysis in tissues of Adam17 hypomorphic and wildtype control C57BL/6 mice.

Publication Title

Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.

Sample Metadata Fields

Sex

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accession-icon GSE79998
Adam17-Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling (aorta)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

Gene expression analysis in tissues of Adam17 hypomorphic and wildtype control C57BL/6 mice.

Publication Title

Adam17 Deficiency Promotes Atherosclerosis by Enhanced TNFR2 Signaling in Mice.

Sample Metadata Fields

Sex

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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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