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accession-icon GSE63068
Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic fatty liver disease
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 72 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.

Sample Metadata Fields

Age, Specimen part, Disease

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accession-icon GSE63027
Expression data from GNMT and MAT1A knockout models that develop all the stages of non-alcoholic fatty liver disease including hepatocellular carcinoma [GNMT_MAT1A_3&8_months]
  • organism-icon Mus musculus
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon

Description

Liver global gene expression patterns of 9 GNMT-knockout mice histopathologically determined to have non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) together with 10 MAT1A-knockout mice histopathologically determined to have steatosis and NASH. All these have their respective wild type patterns. These were analyzed to define signatures to study the pathogenesis of NAFLD-derived HCC, explore which subtypes of cancers can be investigated using mouse models and define a signature of HCC differential survival that can be used to characterize HCC subtypes of different survival derived from mixed etiologies.

Publication Title

Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease.

Sample Metadata Fields

Age, Specimen part, Disease

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accession-icon GSE102850
The gene expression profiles in BALB/3T3 cells during ECTV infection
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

Ectromelia virus (ECTV) has emerged as a valuable model for investigating the host-orthopoxvirus relationship as it relates to pathogenesis and the immune response. We analyzed the transcriptional signatures of BALB/3T3 cells at different times after infection with Ectromelia virus. Mouse Genome 430 2.0 arrays were used to analyze global changes in gene transcripts to generate a pool of genes that was a fold change cut-off of 1.5 or 0.5 in infected samples versus non-infected samples.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line, Time

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accession-icon GSE100644
Comparison of host gene expression profiles in spleen tissues of genetically susceptible and resistant mice during ECTV infection
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

Ectromelia virus (ECTV) has emerged as a valuable model for investigating the host-orthopoxvirus relationship as it relates to pathogenesis and the immune response. ECTV causes mousepox in most strains of mice, including BALB/c and DBA/2, and these are therefore classified as susceptible mice. Conversely, C57BL/6 and certain 129 strains display limited pathology and a very low mortality, and are thus classified as resistant. To understand the host genetic factors of different mouse strains in response to ECTV infection, we carried out a microarray analysis using Affymetrix Gene-Chip Mouse Genome Arrays of spleen tissues from BALB/c and C57BL/6 mice at 3 and 10 days post-ECTV infection.

Publication Title

Comparison of Host Gene Expression Profiles in Spleen Tissues of Genetically Susceptible and Resistant Mice during ECTV Infection.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon GSE62887
Expression data from haploid and diploid epiblast stem cells
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Haploid pluripotent stem cells, such as haploid embryonic stem cells (haESCs), facilitate the genetic study of recessive traits. In vitro, fish haESCs maintain haploidy in both undifferentiated and differentiated states, but whether mammalian haESCs can preserve pluripotency in the haploid state has not been tested. Here, we report that mouse haESCs can differentiate in vitro into haploid epiblast stem cells (haEpiSCs), which maintain an intact haploid genome, unlimited self-renewal potential, and durable pluripotency to differentiate into various tissues in vitro and in vivo. Mechanistically, the maintenance of self-renewal potential depends on the Activin/bFGF pathway. We further show that haEpiSCs can differentiate in vitro into haploid progenitor-like cells.

Publication Title

Durable pluripotency and haploidy in epiblast stem cells derived from haploid embryonic stem cells in vitro.

Sample Metadata Fields

Specimen part

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accession-icon GSE107292
Expression data and genome-wide maps of chromatin in Phf8 knock out and wild type mice
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Phf8 histone demethylase deficiency causes cognitive impairments through the mTOR pathway.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE107210
Expression data from hippocampus of Phf8 knock out and wild type mice
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon

Description

We used microarrays to detail the global programme gene expression of Phf8 knock out and wild type mice

Publication Title

Phf8 histone demethylase deficiency causes cognitive impairments through the mTOR pathway.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE52358
Gene expression profiling of the tongue bud from Alk5 mutant mouse models
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the tongue bud from mice at embryonic day E13.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions.

Publication Title

ALK5-mediated transforming growth factor β signaling in neural crest cells controls craniofacial muscle development via tissue-tissue interactions.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE52357
Gene expression profiling of the mandibular arch from Alk5 mutant mouse models
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the mandibular arch from mice at embryonic day E11.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions.

Publication Title

ALK5-mediated transforming growth factor β signaling in neural crest cells controls craniofacial muscle development via tissue-tissue interactions.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE83326
Hepatic gene expression data from cadmium-exposed mice
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon

Description

Environmental cadmium, with a high average dietary intake, is a severe public health risk. However, the long-term health implications of environmental exposure to cadmium in different life stages remain unclear.

Publication Title

Sex-Dependent Effects of Cadmium Exposure in Early Life on Gut Microbiota and Fat Accumulation in Mice.

Sample Metadata Fields

Sex, 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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