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accession-icon GSE21368
Myocardial expression data from ketogenic diet-fed mice
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon

Description

Specific pathogen free wild-type C57Bl/6 male mice fed ketogenic diet (Bio-Serv AIN-76-A) for 4 weeks

Publication Title

Adaptation of myocardial substrate metabolism to a ketogenic nutrient environment.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE14366
Analysis of the retinal gene expression after hypoxic preconditioning identifies candidate genes for neuroprotection
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

Neuroprotective therapies for retinal degeneration may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning stabilizes the transcription factor HIF-1 in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration.

Publication Title

Analysis of the retinal gene expression profile after hypoxic preconditioning identifies candidate genes for neuroprotection.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17667
Pou5f1 transcription targets in zebrafish
  • organism-icon Danio rerio
  • sample-icon 3 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Zebrafish Pou5f1-dependent transcriptional networks in temporal control of early development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17657
Experiment 4: Affymetrix validation array
  • organism-icon Danio rerio
  • sample-icon 3 Downloadable Samples
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Description

Zebrafish embryo were analyzed at 30 and 60 % epiboly for changes in transcriptome of wild-type and MTspg mutant embryos

Publication Title

Zebrafish Pou5f1-dependent transcriptional networks in temporal control of early development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE30140
Expression data from livers of F2 mice (C57BL/6 X DBA/2) deficient in leptin receptor (db/db)
  • organism-icon Mus musculus
  • sample-icon 435 Downloadable Samples
  • Technology Badge Icon

Description

In several models of obesity-induced diabetes, increased lipid accumulation in the liver has been associated with decreased diabetes susceptibility. For instance, deficiency in leptin receptor (db/db) leads to hyperphagia and obesity in both C57BL/6 and C57BLKS mice but, only on the C57BLKS background do the mice develop beta-cell loss leading to severe diabetes while C57BL/6 mice are relatively resistant. Liver triglyceride levels in the resistant C57BL/6 mice are 3 to 4 fold higher than in C57BLKS.

Publication Title

Systems genetics of susceptibility to obesity-induced diabetes in mice.

Sample Metadata Fields

Sex, Age

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accession-icon GSE108640
Ichthyosis molecular fingerprinting shows profound Th17-skewing and a unique barrier genomic signature
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The purpose of this study was to analyze the genomic signatures and profiles of skin from ichthyosis (various subtypes) vs. healthy patients. The analysis strategy was to study differentially expressed genes common to the ichthyosis shared phenotype, as well as individual ichthyosis subtypes, and compare and contrast to the genomic profiles of atopic dermatitis and psoriasis.

Publication Title

Ichthyosis molecular fingerprinting shows profound T<sub>H</sub>17 skewing and a unique barrier genomic signature.

Sample Metadata Fields

Age, Specimen part, Disease

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accession-icon GSE71090
Expression data from isogenic Pten WT or KO mouse T-ALLs
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Metabolic reprogramming induces resistance to anti-NOTCH1 therapies in T cell acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE71087
Expression data from isogenic Pten WT or KO mouse T-ALLs treated with DBZ or DMSO
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo.

Publication Title

Metabolic reprogramming induces resistance to anti-NOTCH1 therapies in T cell acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE34552
Expression data from mouse kidney tissue
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

The role of the renin-angiotensin system in chronic kidney disease involves multiple peptides and receptors. Exerting antipodal pathophysiological mechanisms, renin inhibition and AT1 antagonism ameliorate renal damage.

Publication Title

AT1 antagonism and renin inhibition in mice: pivotal role of targeting angiotensin II in chronic kidney disease.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE46990
Gene expression changes induced by expression of MN1 deletion mutants in murine bone marrow cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Extensive molecular profiling of leukemias and preleukemic diseases has revealed that distinct clinical entities, like acute myeloid (AML) and T-lymphoblastic leukemia, share the same pathogenetic mutations. It is not well understood how the cell of origin, accompanying mutations, extracellular signals or structural differences in a mutated gene determine the phenotypic identity of the malignant disease. We studied the relationship of different protein domains of the MN1 oncogene and their effect on the leukemic phenotype, building on the ability of MN1 to induce leukemia without accompanying mutations. We found that the most C-terminal domain of MN1 was required to block myeloid differentiation at an early stage, and deletion of an extended C-terminal domain resulted in loss of myeloid identity and cell differentiation along the T-cell lineage in vivo. Megakaryocytic/erythroid lineage differentiation was blocked by the most N-terminal domain. In addition, the N-terminus was required for proliferation and leukemogenesis in vitro and in vivo through upregulation of HoxA9, HoxA10 and Meis2. Our results provide evidence that a single oncogene can modulate cellular identity of leukemic cells based on its active domains. It is therefore likely that different mutations in the same oncogene may impact cell fate decisions and phenotypic appearance of malignant diseases.

Publication Title

Cell fate decisions in malignant hematopoiesis: leukemia phenotype is determined by distinct functional domains of the MN1 oncogene.

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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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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