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accession-icon GSE15182
Comparison of ATG5-/- Bcl-2 tumors expressing p62-GFP versus those expressing EGFP
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Autophagy is a starvation response that facilitates cell survival under metabolic stress and yet defects in autophagy promote tumorigenesis. While the role of understarvation is relatively clearer, its mechanistic role in tumorigenesis is poorly understood. We show that defective autophagy promotes protein damage and accumulation of p62, a marker for protein damage accumulation that is cleared through autophagy pathway. The failure to eliminate p62 in autophagy-defective cells, leads to deregulation of cell signalling and gene expression and ultimately promotes tumorigenesis. Thus defective-autophagy is a mechanism for p62 accumulation commonly observed in human tumors.

Publication Title

Autophagy suppresses tumorigenesis through elimination of p62.

Sample Metadata Fields

Cell line

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accession-icon GSE117853
Gene expression and methylation profile of Human non-functional Pancreatic neuroendocrine tumors (PanNETs)
  • organism-icon Homo sapiens
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

ATRX, DAXX or MEN1 mutant pancreatic neuroendocrine tumors are a distinct alpha-cell signature subgroup.

Sample Metadata Fields

Specimen part

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accession-icon GSE117851
Gene expression profile of Human non-functional Pancreatic neuroendocrine tumors (PanNETs)
  • organism-icon Homo sapiens
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Gene expression profiling of PanNETs patients samples were performed to understand genotype to phenotype correlations, novel molecular subtypes and cell of origin

Publication Title

ATRX, DAXX or MEN1 mutant pancreatic neuroendocrine tumors are a distinct alpha-cell signature subgroup.

Sample Metadata Fields

Specimen part

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accession-icon GSE35972
TOV112D cells treated with NSC319726
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Rescuing the function of mutant p53 protein is an attractive cancer therapeutic strategy. Using the NCI anticancer drug screen data, we identified two compounds from the thiosemicarbazone family that manifest increased growth inhibitory activity in mutant p53 cells, particularly for the p53R175 mutant. Mechanistic studies reveal that NSC319726 restores WT structure and function to the p53R175 mutant. This compound kills p53R172H knock-in mice with extensive apoptosis and inhibits xenograft tumor growth in a 175-allele specific mutant p53 dependent manner. This activity depends upon the zinc ion chelating properties of the compound as well as redox changes. These data identify NSC319726 as a p53R175 mutant reactivator and as a lead compound for p53 targeted drug development.

Publication Title

Allele-specific p53 mutant reactivation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE55081
Expression data from yeast wild type (WT) and sod1 strains after treatment with hydrogen peroxide (H2O2)
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

An important cellular defense mechanism against oxidative stress is the induction of genes involved in ROS resistance and DNA damage repair. Under normal conditions, Sod1 is localized mainly in the cytosol. However, we found that Sod1 translocates into the nucleus after oxidative stress.

Publication Title

Superoxide dismutase 1 acts as a nuclear transcription factor to regulate oxidative stress resistance.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE33417
Global analysis of mRNA decay in induced pluripotent stem cells
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Expression data from human induced pluripotent stem cells(iPSCs) and Human foreskin fibroblasts (HFFs) with treatment actinomycin D

Publication Title

Global analysis reveals multiple pathways for unique regulation of mRNA decay in induced pluripotent stem cells.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE35944
The PARN deadenylase targets a discrete set of mRNAs for decay and regulates cell motility in mouse myoblasts
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Almost all cellular mRNAs terminate in a 3 poly(A) tail, the removal of which can induce both translational silencing and mRNA decay. Mammalian cells encode many poly(A)-specific exoribonucleases but their individual roles are poorly understood. Here, we undertook an analysis of the role of PARN deadenylase in mouse myoblasts using global measurements of mRNA decay rates. Our results reveal that a discrete set of mRNAs exhibit altered mRNA decay as a result of PARN depletion and that stabilization is associated with increased poly(A) tail length and translation. We determined that stabilization of mRNAs does not generally result in their increased abundance supporting the idea that mRNA decay is coupled to transcription. Importantly, PARN knockdown has wide ranging effects on gene expression that specifically impact the extracellular matrix and cell migration. Finally, although PARN has its own unique target transcripts it also influences some genes whose expression is modulated by other deadenylases.

Publication Title

The PARN deadenylase targets a discrete set of mRNAs for decay and regulates cell motility in mouse myoblasts.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE21236
Systematic analysis of cis-elements in unstable mRNAs demonstrates that CUGBP1 is a key regulator of mRNA decay in muscle cells
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Systematic analysis of cis-elements in unstable mRNAs demonstrates that CUGBP1 is a key regulator of mRNA decay in muscle cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE21233
Expression data from C2C12 mouse myoblast with treatment actinomycin D
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Dramatic changes in gene expression occur in response to extracellular stimuli and during differentiation. Although transcriptional effects are important, alterations in mRNA decay also play a major role in achieving rapid and massive changes in mRNA abundance. Moreover, just as transcription factor activity varies between different cell types, the factors influencing mRNA decay are also cell-type specific. We have established the rates of decay for over 7000 transcripts expressed in mouse C2C12 myoblasts.

Publication Title

Systematic analysis of cis-elements in unstable mRNAs demonstrates that CUGBP1 is a key regulator of mRNA decay in muscle cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE93426
Global Gene Expression Profiles of Postnatal Myocardium
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The present study was to investigate the differentially expressed genes in 24-hour-old (containing proliferative cardiomyocytes), 7-day-old (containing the burst of proliferative cardiomyocytes), and 10-week-old (containing growth-arrested cardiomyocytes) C57BL/6 mouse hearts using global gene expression profiles.

Publication Title

Global gene expression analysis combined with a genomics approach for the identification of signal transduction networks involved in postnatal mouse myocardial proliferation and development.

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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