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accession-icon GSE21755
Rapamycin effect on Wild Type and TSC deficient Mouse Embryonic Fibroblasts : Time Course
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Aberrant activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a common molecular event in a large variety of pathological settings, including genetic tumor syndromes, cancer, and obesity. However, the cell intrinsic consequences of mTORC1 activation remain poorly defined. Here, we identify global trancriptional changes in TSC1 and TSC2 null MEFs, which exhibit constitutive activation of mTORC1, compared to wild-type littermate control lines. A rapamycin time course is included to determine those changes that are dependent on mTORC1 signaling, revealing mTORC1 induced and repressed transcripts.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line, Time

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accession-icon GSE64762
Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Activating mutations in either KIT or PDGFRA are present in approximately 90% of gastrointestinal stromal tumors (GISTs). Although treatment with the KIT and PDGFR inhibitor imatinib can control advanced disease in about 80% of GIST patients, the beneficial effect is not durable. Here, we report that ligands from the FGF family reduced the effectiveness of imatinib in GIST cells, and FGF2 and FGFR1 are highly expressed in all primary GIST samples examined. The combination of KIT and FGFR inhibition showed increased growth inhibition in imatinib-sensitive GIST cell lines in the presence or absence of added FGF2 in vitro, and delayed tumor regrowth in vivo. In addition, inhibition of mitogen-activated protein kinase (MAPK) signaling by imatinib was not sustained in GIST cells. An extracellular signal-regulated kinase (ERK) rebound occurred through activation of FGF signaling, and was repressed by FGFR1 inhibition. Downregultation of Sprouty proteins played a role in the imatinib-induced feedback activation of FGF signaling in GIST cells.

Publication Title

FGFR-Mediated Reactivation of MAPK Signaling Attenuates Antitumor Effects of Imatinib in Gastrointestinal Stromal Tumors.

Sample Metadata Fields

Cell line

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accession-icon GSE7079
Chronic rat exposure to cigarette smoke
  • organism-icon Rattus norvegicus
  • sample-icon 208 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome U34 Array (rgu34a)

Description

Chronic obstructive pulmonary disease is a smoking-related disease that lacks effective therapies due partly to the poor understanding of disease pathogenesis. The aim of this study was to identify molecular pathways which could be responsible for the damaging consequences of smoking. To do this, we employed recently described bioinformatic methods to analyze differences in global gene expression, which we then related to the pathological changes induced by cigarette smoke (CS). Sprague-Dawley rats were exposed to whole-body CS for 1 day and for various periods up to 8 months.

Publication Title

Comprehensive gene expression profiling of rat lung reveals distinct acute and chronic responses to cigarette smoke inhalation.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE67326
GDF11 is a myokine that inhibits muscle differentiation and induces atrophy during regeneration
  • organism-icon Homo sapiens
  • sample-icon 50 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Age-related frailty may in part be due to a decreased competency in skeletal muscle regeneration. The role of the closely related TGFbeta amily molecules myostatin and GDF11 in regeneration is unclear. The commercially available antibody which in a prior report was used to demonstrate an age-related decrease in GDF11 was found to detect both GDF11 and myostatin, and with this reagent it appears that the combination of GDF11 and myostatin increases with age in serum. Mechanistically, GDF11 and myostatin induce SMAD2/3 phosphorylation, and both inhibit myoblast differentiation and regulate identical downstream signaling. GDF11 injected into adult mice in a model of regeneration induces an increase in smaller fibers and a decrease in satellite cell expansion. There are no signs of benefit from GDF11 to regeneration. Thus, GDF11 appears to be an age-associated myokine that inhibits muscle differentiation, and is thus a target for blockade to treat frailty

Publication Title

GDF11 Increases with Age and Inhibits Skeletal Muscle Regeneration.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE63664
Gene expression induced by DOT1L and Menin inhibition in cell line models of leukemia
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 56 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression upon DOT1L inhibition, or Menin inhibition, or a combination of DOT1L and Menin inhibiting agents, was assessed in several MLL-rearranged human cell lines and a mouse model of MLL-AF9 leukemia.

Publication Title

Complementary activities of DOT1L and Menin inhibitors in MLL-rearranged leukemia.

Sample Metadata Fields

Cell line

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accession-icon GSE45577
Profiling of glycerol- and CTX-induced models of muscle regeneration in mice
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Utilizing glycerol and cardiotoxin (CTX) injections in the tibialis anterior muscles of M. musculus provides models of skeletal muscle damages followed by skeletal muscle regeneration. In particular, glycerol-induced muscle regeneration is known to be associated with ectopic adipogenesis. We characterized genome-wide expression profiles of tibialis anterior muscles from wild-type mice injured by either glycerol or CTX injection. Our goal was to detect gene expression changes during the time course of glycerol-induced and CTX-induced muscle regeneration models, that can lead to ectopic adipocyte accumulation.

Publication Title

Genomic profiling reveals that transient adipogenic activation is a hallmark of mouse models of skeletal muscle regeneration.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE21912
The Polycomb Group Protein Bmi-1 is essential for the growth of Multiple Myeloma cells
  • organism-icon Homo sapiens
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The RPMI-8226 human multiple myeloma cell line was stably infected with either a validated shRNA against BMI1 or a control shRNA. RNA was prepared from these lines, +/- doxycycline induction and at various time points post-induction. Samples were hybridized on the Affymetrix U133plus2 human genome expression microarray.

Publication Title

The Polycomb group protein Bmi-1 is essential for the growth of multiple myeloma cells.

Sample Metadata Fields

Cell line

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accession-icon GSE22007
Targeting resistance to Smoothened antagonists by inhibiting the PI3K pathway
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE56465
Comparison of haploid and diploid clones of KBM7 cancer cell line
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The series were performed to study the changes in gene expression upon diploidization of KBM7 cancer (CML) cell line. The line can exist either as a clone with 24 chromosomes (nearly haploid) or with

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE22456
low and high aerobic capacity rats exposed to cigarette smoke, lung tissue
  • organism-icon Rattus norvegicus
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Low aerobic exercise capacity increases susceptibility to smoking-induced inflammation and tissue damage

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
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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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