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accession-icon GSE79930
Activation of GCN2 by Ribosome Stalling Links Translation Elongation with Translation Initiation
  • organism-icon Mus musculus
  • sample-icon 24 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

Activation of GCN2 kinase by ribosome stalling links translation elongation with translation initiation.

Alternate Accession IDs

E-GEOD-79930

Sample Metadata Fields

Age

View Samples
accession-icon GSE79926
Examination of gene expression in cerebellum and hippocampus for mouse C57BL/6J WT and nmf205-/-
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Ribosome stalling during translation has recently been shown to cause neurodegeneration, yet the signaling pathways triggered by stalled elongation complexes are unknown. To investigate these pathways we analyzed the brain of B6J-nmf205-/- mice in which neuronal elongation complexes are stalled at AGA codons due to deficiencies in a tRNA Arg(UCU) tRNA and GTPBP2, a mammalian ribosome rescue factor. Increased levels of phosphorylation of eIF2 (Ser51) were detected prior to neurodegeneration in these mice and transcriptome analysis demonstrated activation of ATF4, a key transcription factor in the integrated stress response (ISR) pathway. Genetic experiments showed that this pathway was activated by the eIF2 kinase, GCN2, in an apparent deacylated tRNA-independent fashion. Further we found that the ISR attenuates neurodegeneration in B6J-nmf205-/- mice, underscoring the importance of cellular and stress context on the outcome of activation of this pathway. These results demonstrate the critical interplay between translation elongation and initiation in regulating neuron survival during cellular stress.

Publication Title

Activation of GCN2 kinase by ribosome stalling links translation elongation with translation initiation.

Alternate Accession IDs

E-GEOD-79926

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13854
Expression profiling of the host and the Ovine Herpesvirus 2 pathogen during malignant catarrhal fever of cattle
  • organism-icon Bos taurus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Malignant catarrhal fever of cattle is associated with low abundance of IL-2 transcript and a predominantly latent profile of ovine herpesvirus 2 gene expression.

Alternate Accession IDs

E-GEOD-13854

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE13852
Expression profiling of Bos taurus lymph nodes upon infection with Ovine Herpesvirus 2
  • organism-icon Bos taurus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Bovine Genome Array (bovine)

Description

We hypothesized that the relative abundances of host cell transcripts in lymph nodes of animals with malignant catarrhal fever (MCF), compared to healthy controls, may be used to identify pathways that may help to explain the pathogenesis of MCF. Therefore, an abundance of host cell gene expression patterns in lymph nodes of animals with MCF and healthy controls were analyzed by microarray. Indeed, a vast number of genes related to inflammatory processes, lymphocyte activation, cell proliferation and apoptosis were detected at different abundances. However, the IL-2 transcript was eminent among the transcripts, which were, compared to healthy controls, less abundant in animals with MCF. Compared to healthy cattle, bovines with MCF appear to mimic an IL-2 knockout phenotype that has been described in mice. This supports the hypothesis that immunopathogenic events are linked to the pathogenesis of MCF. IL-2-deficiency may play an important role in the process.

Publication Title

Malignant catarrhal fever of cattle is associated with low abundance of IL-2 transcript and a predominantly latent profile of ovine herpesvirus 2 gene expression.

Alternate Accession IDs

E-GEOD-13852

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE15078
Fog2 regulation of gene expression in the adult heart
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

MHCaCre induced knockout of Fog2flox.

Publication Title

Fog2 is critical for cardiac function and maintenance of coronary vasculature in the adult mouse heart.

Alternate Accession IDs

E-GEOD-15078

Sample Metadata Fields

Sex, Specimen part, Treatment

View Samples
accession-icon GSE58220
Expression data from primary term human decidual cells treated with interleukin-1-beta for 6 hours.
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Preterm birth is an important unsolved clinical problem. Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities. In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment. Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions. Using monolayer cultures of human decidual cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge.

Publication Title

Inflammatory gene networks in term human decidual cells define a potential signature for cytokine-mediated parturition.

Alternate Accession IDs

E-GEOD-58220

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE26315
Expression data from human amnion mesenchymal cells treated with interleukin-1-beta for 1hr and 8hr
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

Premature birth continues to be a challenging pregnancy complication, and a body of literature indicates that inflammation can contribute to premature delivery by converting a receptive uterine environment to a hostile one. Cytokines have been demonstrated to provoke up-regulation of inflammatory genes (e.g. interleukin-1, 6, and 8, tumor necrosis factor-alpha, cyclooxygenase-2, and microsomal prostaglandin E synthase-1).

Publication Title

Inflammatory gene regulatory networks in amnion cells following cytokine stimulation: translational systems approach to modeling human parturition.

Alternate Accession IDs

E-GEOD-26315

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE5959
Expression differences in the liver of a congenic mouse with low serum IGF-1
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Several studies have shown that bone mineral density (BMD), a clinically measurable predictor of osteoporotic fracture, is the sum of genetic and environmental influences. In addition, serum IGF-1 levels have been correlated to both BMD and fracture risk. We previously identified a Quantitative Trait Locus (QTL) for Bone Mineral Density (BMD) on mouse Chromosome (Chr) 6 that overlaps a QTL for serum IGF-1. The B6.C3H-6T (6T) congenic mouse is homozygous for C57BL/6J (B6) alleles across the genome except for a 30 cM region on Chr 6 that is homozygous for C3H/HeJ (C3H) alleles. This mouse was created to study biology behind both the BMD and the serum IGF-1 QTLs and to identify the gene(s) underlying these QTLs. Female 6T mice have lower BMD and lower serum IGF-1 levels at all ages measured. As the liver is the major source of serum IGF-1, we examined differential expression in the livers of fasted female B6 and 6T mice by microarray.

Publication Title

A chromosomal inversion within a quantitative trait locus has a major effect on adipogenesis and osteoblastogenesis.

Alternate Accession IDs

E-GEOD-5959

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE117775
Effect of DGAT loss on hypoxic tumor cells growing under serum-deprived conditions
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

The metabolic enzyme diglyceride acyltransferase (DGAT) is responsible for the synthesis of triglycerides. Loss of its expression may sensitize cells to conditions of nutrient and oxygen that are commonly present in tumors. This study is designed to identify stress response pathways that may be induced following the shRNA-mediated knockdown of the two genes coding for the DGAT enzymes. In vitro growth conditions lacking serum and oxygen were used to mimic growth conditions commonly found in poorly perfused tumor domains

Publication Title

Triglycerides Promote Lipid Homeostasis during Hypoxic Stress by Balancing Fatty Acid Saturation.

Alternate Accession IDs

E-GEOD-117775

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE117774
Effect of DGAT knockdown on gene expression in A498 xenograft tumors
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

The metabolic enzyme diglyceride acyltransferase (DGAT) is responsible for the synthesis of triglycerides. Loss of its expression may sensitize cells to conditions of nutrient and oxygen that are commonly present in tumors. This study is designed to identify stress response pathways that may be induced following the shRNA-mediated knockdown of the two genes coding for the DGAT enzymes.

Publication Title

Triglycerides Promote Lipid Homeostasis during Hypoxic Stress by Balancing Fatty Acid Saturation.

Alternate Accession IDs

E-GEOD-117774

Sample Metadata Fields

Specimen part, Treatment

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)

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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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