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accession-icon GSE39375
Polysome profiling in liver identifies dynamic regulation of endoplasmic reticulum translatome by obesity and fasting
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Obesity-associated metabolic complications are generally considered to emerge from abnormalities in carbohydrate and lipid metabolism, whereas the status of protein metabolism is not well studied. Here, we performed comparative polysome and associated transcriptional profiling analyses to study the dynamics and functional implications of endoplasmic reticulum (ER)-associated protein synthesis in the mouse liver under conditions of obesity and nutrient deprivation.

Publication Title

Polysome profiling in liver identifies dynamic regulation of endoplasmic reticulum translatome by obesity and fasting.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE17239
MYC Transactome Mapped by Global Array-based Nuclear Run-on (ANRO - Affymetrix)
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

We describe and illustrate the use of a method to measure nascent nuclear gene transcription with an Array-based Nuclear Run-On (ANRO) assay using commercial microarray platforms.

Publication Title

Time-dependent c-Myc transactomes mapped by Array-based nuclear run-on reveal transcriptional modules in human B cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE12854
Overexpression of PKA regulatory subunits in ovarian cancer cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The regulatory subunit of cAMP-dependent protein kinase (PKA) exists in two isoforms, RI and RII, which distinguish the PKA isozymes, type I (PKA-I) and type II (PKA-II). Evidence obtained from a variety of different experimental approaches has shown that the relative levels of type I and type II PKA in cells can play a major role in determining the balance between cell growth and differentiation. RI transfected cells exhibit hyper-proliferative growth and RII transfected cells revert to a relatively quiescent state. Profiling by microarray revealed equally profound changes in gene expression between RI, RII, and parental OVCAR cells.

Publication Title

Regulatory subunits of PKA define an axis of cellular proliferation/differentiation in ovarian cancer cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE32467
Expression data from wildtype and unc-37 mutant A-class motor neurons in C. elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

In Caenorhabditis elegans, VA and VB motor neurons arise as lineal sisters but synapse with different interneurons to regulate locomotion. VA-specific inputs are defined by the UNC-4 homeoprotein and its transcriptional corepressor, UNC-37/Groucho, which function in the VAs to block the creation of chemical synapses and gap junctions with interneurons normally reserved for VBs. To reveal downstream genes that control this choice, we have employed a cell-specific microarray strategy that has now identified unc-4-regulated transcripts. One of these genes, ceh-12, a member of the HB9 family of homeoproteins, is normally restricted to VBs. We show that expression of CEH-12/HB9 in VA motor neurons in unc-4 mutants imposes VB-type inputs. Thus, this work reveals a developmental switch in which motor neuron input is defined by differential expression of transcription factors that select alternative presynaptic partners. The conservation of UNC-4, HB9, and Groucho expression in the vertebrate motor circuit argues that similar mechanisms may regulate synaptic specificity in the spinal cord.

Publication Title

UNC-4 represses CEH-12/HB9 to specify synaptic inputs to VA motor neurons in C. elegans.

Sample Metadata Fields

Specimen part

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accession-icon GSE26719
Gene expression analysis of dendritic cells from normal or tumor bearing prostates
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Tumors cause the induction or repression of many genes associated with inflammation. To investigate the up and down regulation of genes associated with immune stimulation or immune tolerance RNA was isolated from dendritic cells from normal or tumor bearing prostate for microarray analysis.

Publication Title

FOXO3 programs tumor-associated DCs to become tolerogenic in human and murine prostate cancer.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE26747
Gene expression analysis of dendritic cells from normal or tumor sections of human prostates
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Tumors cause the induction or repression of many genes associated with inflammation. To investigate the up and down regulation of genes associated with immune stimulation or immune tolerance RNA was isolated from dendritic cells from normal or tumor bearing prostate for microarray analysis.

Publication Title

FOXO3 programs tumor-associated DCs to become tolerogenic in human and murine prostate cancer.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE33467
Expression data from liver tissue from Npc1 mouse model
  • organism-icon Mus musculus
  • sample-icon 78 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

We used microarrays to detail the global programme of gene expression underlying the disease progression in the mutant mice compared to their control littermates.

Publication Title

Microarray expression analysis and identification of serum biomarkers for Niemann-Pick disease, type C1.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE15240
Gene expression in laboratory models and primary tumors in Small Cell Lung Cancer
  • organism-icon Homo sapiens
  • sample-icon 45 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression was measured on the Affymetrix platform in primary xenografts, xenograft-derived cell lines, secondary xenografts, normal lung, and primary tumors obtained from chemotherapy naive Small Cell Lung Cancer (SCLC). The SCLC primary xenografts were serially propagated in vivo in immunodeficient mice. Cell lines were derived from each xenograft and grown for 6 months using conventional tissue culture conditions. Secondary xenografts were obtained from cell cultures by re-implantation in immunodeficient mice. Such SCLC laboratory models were analyzed along with conventional SCLC cell lines and the derivative secondary xenografts, with normal lung and primary tumors, to assess irreversible gene expression changes induced by culturing conditions.

Publication Title

A primary xenograft model of small-cell lung cancer reveals irreversible changes in gene expression imposed by culture in vitro.

Sample Metadata Fields

Disease, Disease stage, Cell line

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accession-icon GSE19168
Expression profiling analysis of mouse E10.5 Magoh mutant brain cortices
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Human brain structure and size requires regulated division of neural stem cells (NSCs). NSCs undergo precise divisions to self-renew and to produce intermediate neural progenitors (INPs) and neurons. The factors that regulate NSC divisions remain poorly understood, as do mechanistic explanations of how aberrant NSC division causes reduced brain size, as seen in microcephaly. Here we demonstrate that Magoh, a component of the core exon junction complex (EJC) that binds spliced RNA, controls cerebral cortical size by regulating NSC division. Magoh haploinsufficiency causes microcephaly due to INP depletion, neuronal apoptosis, and improper mitotic spindle orientation. Defective mitosis underlies these phenotypes as depletion of EJC components disrupts mitotic spindle integrity, chromosome number and genomic stability. We show that an essential function of Magoh is to regulate expression of the human microcephaly protein, LIS1, and that Lis1 addition rescues neurogenesis defects caused by Magoh knockdown, thus providing a genetic explanation for the microcephaly. This study uncovers new requirements for the EJC in brain development, NSC maintenance, mitosis and chromosome stability, thus implicating this complex in the pathogenesis of microcephaly.

Publication Title

The exon junction complex component Magoh controls brain size by regulating neural stem cell division.

Sample Metadata Fields

Specimen part

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accession-icon GSE99926
Gene expression data from primary human hepatocytes treated with GGF2 for 6, 24, or 72 h or 24 h with a 48 h washout.
  • organism-icon Homo sapiens
  • sample-icon 91 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

GGF2 is a recombinant human neuregulin-1 in development for chronic heart failure. Phase 1 clinical trials of GGF2 were put on hold when transient elevations in serum aminotransferases and total bilirubin were observed in 2 of 43 subjects receiving GGF2. However, aminotransferase elevations were modest and not typical of liver injury sufficient to result in elevated serum bilirubin. Several translational approaches were used to understand the liver response associated with GGF2.

Publication Title

Transient Changes in Hepatic Physiology That Alter Bilirubin and Bile Acid Transport May Explain Elevations in Liver Chemistries Observed in Clinical Trials of GGF2 (Cimaglermin Alfa).

Sample Metadata Fields

Treatment

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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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