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accession-icon GSE62694
Mutant p53 in fallopian tube epithelium and high-grade serous cancer formation
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Ovarian cancer is the fifth leading cause of cancer death among US women. Evidence supports the hypothesis that high-grade serous ovarian cancers (HGSC) may originate in the distal end of the fallopian tube. Although a heterogeneous disease, 96% of HGSC contain mutations in p53. In addition, the p53 signature, or overexpression of p53 protein (usually associated with mutation), is a potential precursor lesion of fallopian tube derived HGSC suggesting an essential role for p53 mutation in early serous tumorigenesis. To further clarify p53-mutation dependent effects on cells, murine oviductal epithelial cells (MOE) were stably transfected with a construct encoding for the R273H DNA binding domain mutation in p53, the most common mutation in HGSC. Mutation in p53 was not sufficient to transform MOE cells, but did significantly increase cell migration. A similar p53 mutation in murine ovarian surface epithelium (MOSE), another potential progenitor cell for serous cancer, was not sufficient to transform the cells nor change migration suggesting tissue specific effects of p53 mutation. Microarray data confirmed expression changes in pro-migratory genes in p53R273H MOE compared to parental cells, which could be reversed by suppressing Slug expression. Combining p53R273H with KRASG12V activation caused transformation of MOE into high-grade sarcomatoid carcinoma when xenografted into nude mice. Elucidating the specific role of p53R273H in the fallopian tube will improve understanding of changes at the earliest stage of transformation and could help develop chemopreventative strategies to prevent the accumulation of additional mutations and reverse progression of the p53 signature thereby, improving survival rates.

Publication Title

Mutant p53 expression in fallopian tube epithelium drives cell migration.

Sample Metadata Fields

Specimen part

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accession-icon GSE115276
Maternal care boosted by paternal imprinting in mammals
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Previous work has suggested that the imprinted gene Phlda2 regulates the signalling function of the placenta by modulating the size of the endocrine compartment. This study investigated the affect that Phlda2 mutant placenta has upon the brains of the wildtype dams carrying different placenta and consequently offspring.

Publication Title

Maternal care boosted by paternal imprinting in mammals.

Sample Metadata Fields

Specimen part

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accession-icon SRP049674
Epigenomic Signatures of Neuronal Diversity in the Mammalian Brain
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

We developed an affinity purification approach to isolate tagged nuclei in mice (similar to INTACT; [Deal R.B. and Henikoff S. A simple method for gene expression and chromatin profiling of individual cell types within a tissue. Dev. Cell 18,1030-1040. (2010)]) and used it to characterize genome-wide patterns of transcription, DNA methylation, and chromatin accessibility in 3 major neuron classes of the neocortex (excitatory pyramidal neurons, parvalbumin (PV)-positive GABAergic interneurons, and vasoactive intestinal peptide (VIP)-positive GABAergic interneurons). By combining cell purification and integrative analysis, our findings relate the phenotypic and functional complexity of neocortical neurons to their underlying transcriptional and epigenetic diversity. Overall design: RNA-seq, MethylC-seq, ATAC-seq, and ChIP-seq for histone modifications using INTACT-purified nuclei from the mouse neocortex

Publication Title

Epigenomic Signatures of Neuronal Diversity in the Mammalian Brain.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE17880
Expression data from B6C3F1 mice treated with 2-butoxyethanol and reduced oxygen
  • organism-icon Mus musculus
  • sample-icon 82 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

The role of hypoxia in 2-butoxyethanol-induced hemangiosarcoma.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE17266
Expression data from B6C3F1 mice treated with baclofen
  • organism-icon Mus musculus
  • sample-icon 59 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mice were treated with either 100mg/kg baclofen or 0.5% methylcellulose alone by oral gavage for 1 or 5 days.

Publication Title

The role of hypoxia in 2-butoxyethanol-induced hemangiosarcoma.

Sample Metadata Fields

Specimen part, Treatment, Time

View Samples
accession-icon GSE17794
Expression data from B6C3F1 mice treated with 2-butoxyethanol
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mice were dosed with 2-BE (900mg/kg) or vehicle by oral gavage and sacrificied either after 4 hours of a single dose or after 7 days of daily dosing.

Publication Title

The role of hypoxia in 2-butoxyethanol-induced hemangiosarcoma.

Sample Metadata Fields

Specimen part, Treatment, Time

View Samples
accession-icon GSE3837
Methylglyoxal treatment of MH-S cell line induces apoptosis and immune response
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mycobacteria-induced apoptosis of macrophages plays an important role in modulation of the host immune response involving TNF-alpha as major cytokine. The underlying mechanisms are still ill-defined. Here, we show for the first time that methylglyoxal (MG) and AGEs levels were elevated during mycobacterial infection of macrophages and that their increased levels mediated mycobacteria-induced apoptotic and immune response of macrophages. Moreover, we show that high levels of AGEs were formed at the sites of pulmonary tuberculosis. This observation represents the first evidence of the potential involvement of AGEs in tuberculosis and in infectious diseases in general. Global gene expression profiling of MG-treated macrophages reveals diversified potential roles of MG in cellular processes, including apoptosis, immune response, and growth regulation. The results of this study provide new insights into intervention strategies to develop therapeutic tools against infectious diseases in which MG and AGE production plays critical roles.

Publication Title

Critical role of methylglyoxal and AGE in mycobacteria-induced macrophage apoptosis and activation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE56427
Pharmacodynamic effects of GLP-1 agonist liraglutide in adolescent, prediabetic pigs
  • organism-icon Sus scrofa
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Porcine Gene 1.0 ST Array (porgene10st)

Description

GLP-1 agonists are potent glucose-lowering agents, however, their effect on adolescent organisms needs to be clarified

Publication Title

Effects of the glucagon-like peptide-1 receptor agonist liraglutide in juvenile transgenic pigs modeling a pre-diabetic condition.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE11035
Effect of 5HTT knockout and heterozygosity in whole mouse lung
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Rationale: While modulation of the serotonin transporter (5HTT) has shown to be a risk factor for pulmonary arterial hypertension for almost 40 years, there is a lack of in vivo data about the broad molecular effects of pulmonary inhibition of 5HTT. Previous studies have suggested effects on inflammation, proliferation, and vasoconstriction. The goal of this study was to determine which of these were supported by alterations in gene expression in serotonin transporter knockout mice. Methods: Eight week old normoxic mice with a 5-HTT knock-out (5HTT-/-) and their heterozygote(5HTT+/-) or wild-type(5HTT+/+) littermates had right ventricular systolic pressure(RVSP) assessed, lungs collected for RNA, pooled, and used in duplicate in Affymetrix array analysis. Representative genes were confirmed by quantitative RT-PCR and western blot. Results: RVSP was normal in all groups. Only 124 genes were reliably changed between 5HTT-/- and 5HTT+/+ mice. More than half of these were either involved in inflammatory response or muscle function and organization; in addition, some matrix, heme oxygenase, developmental, and energy metabolism genes showed altered expression. Quantitative RT-PCR for examples from each major group confirmed changes seen by array, with an intermediate level in 5HTT+/- mice. Conclusions: These results for the first time show the in vivo effects of 5HTT knockout in lungs, and show that many of the downstream mechanisms suggested by cell culture and ex vivo experiments are also operational in vivo. This suggests that the effect of 5HTT on pulmonary vascular function arises from its impact on several systems, including vasoreactivity, proliferation, and immune function.

Publication Title

Gene expression in lungs of mice lacking the 5-hydroxytryptamine transporter gene.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE108113
Shared molecular targets in the glomerular and tubulointerstitial transcriptomes from patients with nephrotic syndrome and ANCA-associated vasculitis
  • organism-icon Homo sapiens
  • sample-icon 275 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

This SuperSeries is composed of the SubSeries listed below. A subset of samples profiled in this analysis were also profiled in Series GSE68127, and GSE104066. Corresponding glomerular transcriptome data can be found under GEO ID: GSE108109.

Publication Title

Metabolic pathways and immunometabolism in rare kidney diseases.

Sample Metadata Fields

Specimen part

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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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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