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accession-icon GSE24451
Knockout of the Acyl CoA binding protein (ACBP) in mice - expression profile from the liver of 21 days old ACBP-/- and +/+ mice.
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

The ACBP knockout were created by targeted disruption of the gene in mice. The expression profiling was performed on liver tissue from ACBP-/- (KO) and +/+ (WT) mice at the age of 21 days, which in our study is the time immediately before weaning. The mice used for this experiment were taken directly away from their mother. Thus, having free access to chow and breast milk until sacrificed at 8-11am

Publication Title

Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.

Sample Metadata Fields

Specimen part

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accession-icon GSE55304
Perinatal malnutrition in male mice influences gene expression in the next generation offspring: Potential role of epigenetics.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Perinatal nutritional imbalances may have long-lasting consequences on health and disease, increasing risk of obesity, insulin resistance, type 2 diabetes or cardiovascular disease. This idea has been conceptualized in the Developmental Origins of Health and Disease Hypothesis (DOHaD). In addition, there is evidence that such early-programmed phenotypes can be transmitted to the following generation(s). It is proposed that, environmentally induced, transmission of disease risk is mediated by epigenetic mechanisms.

Publication Title

In utero undernutrition in male mice programs liver lipid metabolism in the second-generation offspring involving altered Lxra DNA methylation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE12466
Transcriptional signatures of Itk-deficient CD3+, CD4+ and CD8+ T-cells
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional signatures of Itk-deficient CD3+, CD4+ and CD8+ T-cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11261
Study of activity-regulated genes in mouse primary cultured neurons
  • organism-icon Mus musculus
  • sample-icon 42 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Activity-dependent regulation of inhibitory synapse development by Npas4.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE29975
Expression data from FOG1+/- (or FOG1+/+) and FOG1 ki/ki mouse megakaryocyte (Meg)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
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Description

The transcription co-factor FOG1 interacts with the chromatin remodeling complex NuRD to mediate gene activation and gene repression during hematopoiesis. We have generated mice with a targeted mutation in the endogenous Fog1 locus that results in an N-ternimal mutation in FOG1 that disrupts the interaction with NuRD.

Publication Title

Pleiotropic platelet defects in mice with disrupted FOG1-NuRD interaction.

Sample Metadata Fields

Specimen part

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accession-icon GSE14980
Consequences of GATA1 expression in Gata1- G1ME Murine Megakaryocyte/Erythrocyte Progenitor Cell Line
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

G1ME cells are GATA1-deficient murine bipotential megakaryocyte/erythrocyte progenitor cells derived from Gata1-negative murine ES cells. In order to assess the impact of GATA1 on gene regulation and cell differentiation, an expression construct was used to transiently produce high levels of GATA1. Cells transduced with this construct or a vector control were harvested at 18 and 42 hours, and gene expression was analyzed using Affymetrix MOE430 version 2 arrays.

Publication Title

Graded repression of PU.1/Sfpi1 gene transcription by GATA factors regulates hematopoietic cell fate.

Sample Metadata Fields

Cell line

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accession-icon GSE56275
Gene expression differences between prion-resistant and prion-susceptible cells
  • organism-icon Mus musculus
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon

Description

Prions consist of aggregates of abnormal conformers of cellular prion protein (PrPC). They propagate by recruiting host-encoded PrPC although the critical interacting proteins and the reasons for the differences in susceptibility of distinct cell lines and populations are unknown. We derived a lineage of cell lines with markedly differing susceptibilities, unexplained by PrPC expression differences, to identify such factors. We examined the transcriptomes of prion-resistant revertants, isolated from highly susceptible cells, and identified a gene expression signature associated with susceptibility. Several of these genes encode proteins with a role in extracellular matrix (ECM) remodelling, a compartment in which disease-related PrP deposits. Loss-of-function of nine of these genes significantly increased susceptibility. Remarkably, inhibition of fibronectin 1 binding to integrin 8 by RGD peptide inhibited metalloproteinases (MMP)-2/9 whilst increasing prion propagation rates. This indicates that prion replication may be controlled by MMPs at the ECM in an integrin-dependent manner.

Publication Title

Identification of a gene regulatory network associated with prion replication.

Sample Metadata Fields

Treatment

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accession-icon GSE18042
Erythroid differentiation: G1E model
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon

Description

Analysis of erythroid differentiation using Gata1 gene-disrupted G1E ER4 clone cells. Estradiol addition activates an ectopically expressed Gata-1-estrogen receptor fusion protein, triggering synchronous differentiation. 30 hour time course corresponds roughly to late burst-forming unit-erythroid stage (t=0 hrs) through orthochromatic erythroblast stage (t=30 hrs).

Publication Title

Erythroid GATA1 function revealed by genome-wide analysis of transcription factor occupancy, histone modifications, and mRNA expression.

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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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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