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accession-icon GSE102588
Expression data from calvaria of 10-day-old 13del-tg transgenic mice displaying bone overgrowth.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

The ectopic expression of a Col10a1-13del transgene in osteocytes induced ER stress, compromising their differentiation and expression of Sclerostin, resulting in generalized bone overgrowth resembling human crainodiaphyseal chondrodysplasia (CCD).

Publication Title

Activating the unfolded protein response in osteocytes causes hyperostosis consistent with craniodiaphyseal dysplasia.

Sample Metadata Fields

Specimen part

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accession-icon GSE25257
Expression data from wild-type and Zmpste24-/- mouse embryonic fibroblasts (MEFs) at an early passage (passage 3, P3)
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

Zmpste24 is a metalloproteinase processing prelamin A into mature lamin A, a nuclear structure protein. Zmpste24-/- mice which accumulate prelamin A in cells recapitulate accelerated aging phenotypes observed in human premature aging disorder, Hutchinson Gilford progeria sydrome (HGPS). Zmpste24-/- mouse embryonic fibroblasts (MEFs) exhibited genomic instabiliy and accelerated aging at cellular level, which is premature senescence.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE10854
The anti-angiogenic and anti-tumor cell signaling networks of the kringle 1 domain of hepatocyte growth factor (HGFK1)
  • organism-icon Mus musculus, Rattus norvegicus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon

Description

Previously, we have demonstrated that the recombinant adeno-associated virus carrying the kringle domain 1 of hepatocyte growth factor (rAAV-HGFK1) gene is a potential anti-angiogenic approach for the treatment of hepatocellular carcinoma (HCC) and exerts direct inhibition effects on tumor cells. Here, using genome-wide expression profiling technology, coupled with RT-PCR validation, we investigated the differentially expressed genes and proposed the mechanisms involved in HGFK1 anti-angiogenic and anti-tumor cell signaling networks.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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accession-icon GSE99306
Expression data of chondrocytes subpopulations from WT, 13del and 13del:Chop-/- mice at P10 stage
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
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Description

The human metaphyseal chondrodysplasia type Schmid is an autosomal dominant disorder associated with mutations in COL10A1 gene that result in ER retention of misfolded alpha(X) collagen in hypertrophic chondrocytes (HCs). In a MCDS transgenic mouse model (13del), we have previously implicated HC response and adaptation to ER stress as the underlying molecular pathogenesis of the disease.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE32082
DNA methylation profiling of embryonic stem cell differentiation into the three germ layers
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

DNA methylation profiling of embryonic stem cell differentiation into the three germ layers.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE111579
Effects of long-term intake of a yogurt fermented with Lactobacillus delbrueckii subsp. bulgaricus 2038 and Streptococcus thermophilus 1131 on mice
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Effects of long-term intake of a yogurt fermented with Lactobacillus delbrueckii subsp. bulgaricus 2038 and Streptococcus thermophilus 1131 on mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE10634
Aquaporin-11 knockout effect on kidney
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

Aquaporin-11 (AQP11), a new member of the aquaporin family, is localized in the endoplasmic reticulum (ER). Aqp11/ mice neonatally suffer from polycystic kidneys derived from the proximal tubule. Its onset is proceeded by the vacuolization of ER. However, the mechanism for the formation of vacuoles and the development of cysts remain to be clarified. Here, we show that Aqp11/ mice and polycystic kidney disease animals share a common pathogenic mechanism of cyst formation.

Publication Title

Aquaporin-11 knockout mice and polycystic kidney disease animals share a common mechanism of cyst formation.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE16110
Altered mouse mammary gland gene expression and tumor growth following chronic social isolation
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon

Description

Clinical studies have revealed that social support improves the outcome of cancer patients while epidemiological studies suggest that social isolation increases the risk of death associated with several chronic diseases. However, the precise biological consequences of an unfavorable social environment have not been defined. To do so, robust, reproducible pre-clinical models are needed to study the mechanisms whereby an adverse environment impacts on gene expression and cancer biology. Because random assignment of inbred laboratory mice to well-defined social environments allows accurate and repeated measurements of behavioral and endocrine parameters, transgenic mice provide a pre-clinical framework with which to begin to determine gene-environment mechanisms. In this study, we found that female C3(1)/SV40 T-antigen mice deprived of social interaction from weaning exhibited increased expression of genes encoding key metabolic pathway enzymes in the pre-malignant mammary gland. Chronic social isolation was associated with upregulated fatty acid synthesis and glycolytic pathway gene expression - both pathways known to contribute to increased breast cancer growth. Consistent with the expression of metabolic genes, isolated mice subsequently developed significantly larger mammary gland tumors compared to group-housed mice. Endocrine evaluation confirmed that isolated mice developed a heightened corticosterone stress response compared to group-housed mice. Together, these transdisciplinary studies show for the first time that an adverse social environment is associated with altered mammary gland gene expression and tumor growth. Moreover, the identification of specific alterations in metabolic pathways favoring tumor growth suggests potential molecular biomarkers and/or targets (e.g. fatty acid synthesis) for preventive intervention in breast cancer.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE109518
Id2-deficient NK cells acquire a nave-like fate
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcription factor ID2 prevents E proteins from enforcing a naïve T lymphocyte gene program during NK cell development.

Sample Metadata Fields

Specimen part

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accession-icon GSE18322
Gene Expression Analysis of Ara-C Resistance in AML
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Using two independently derived murine BXH2 cell lines, Ara-C resistant derivatives were developed by exposure to increasing concentrations of Ara-C. Microarray analysis comparing the Ara-C resistant cells to their Ara-C sensitive parental cell lines identified potential genes involved in Ara-C resistance.

Publication Title

Deoxycytidine kinase is downregulated in Ara-C-resistant acute myeloid leukemia murine cell lines.

Sample Metadata Fields

Specimen part, Cell line

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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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