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accession-icon GSE56183
Integrated miRNA-mRNA analysis revealing the potential roles of miRNAs in chordomas
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Emerging evidence suggests that microRNAs (miRNAs) are crucially involved in tumorigenesis and that paired expression profiles of miRNAs and mRNAs can be used to identify functional miRNA-target relationships with high precision.However, no studies have applied integrated analysis to miRNA and mRNA profiles in chordomas.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE54992
Expression data from peripheral blood
  • organism-icon Homo sapiens
  • sample-icon 38 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

C1q expression increases significantly in the peripheral blood of patients with active tuberculosis compared to healthy controls and individuals with latent TB infection. The percentage of C1q-expressing CD14 positive cells is significantly increased in active TB patients. C1q expression in the peripheral blood correlates with sputum smear positivity in tuberculosis patients and is reduced after anti-tuberculosis chemotherapy. Notably, receiver operating characteristic analysis showed that C1qC mRNA levels in peripheral blood efficiently discriminate active from latent tuberculosis infection and healthy controls. Additionally, C1qC protein level in pleural effusion shows improved power in discriminating tuberculosis from non-tuberculosis pleurisy when compared to other inflammatory markers, such as IL-6 and TNF-

Publication Title

Increased complement C1q level marks active disease in human tuberculosis.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE56649
Expression data from active rheumatoid arthritis patients and healthy control.
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Rheumatoid arthritis (RA) is a systemic autoimmune disease and its underlying molecular mechanisms are still poorly understood. Previously a CD4 T-cell microarray study has only focused arthritis patients. We aimed to compare the molecular profiles of active RA versus healthy control in CD4 T cells.

Publication Title

CD4 T-cell transcriptome analysis reveals aberrant regulation of STAT3 and Wnt signaling pathways in rheumatoid arthritis: evidence from a case-control study.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE22331
Expression data from ejaculated spermatozoa of normozoospermic and asthenozoospermic men
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of ejaculated spermatozoav from normozoospermic men and asthenozoospermic men. Some of genes were up-regulated or down-regulated in asthenozoospermia, and their abnormal expression were the causes of the impaired sperm motility. Results provide insight into the mechanisms by which asthenozoospermia is controlled.

Publication Title

Functional expression of ropporin in human testis and ejaculated spermatozoa.

Sample Metadata Fields

Specimen part

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accession-icon GSE83284
Expression data of osteogenic differentiated cartilage endplate-derived stem cells (CESCs) under hypoxia or normoxia
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Cartilage endplate-derived stem cells (CESCs) with chondro-osteogenic differentiation capacity may be responsible for the balance of chondrification and ossification in cartilage endplate (CEP). CEP is an avascular and hypoxic tissue, and hypoxia could inhibit the osteogenic differentiation of CESCs.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE73771
EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In proliferating cells, where most Polycomb repressive complex 2 (PRC2) studies have been performed, gene repression is associated with PRC2 trimethylation of H3K27 (H3K27me3). However, it is uncertain whether PCR2 writing of H3K27me3 is mechanistically required for gene silencing. Here we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (Embryonic Ectoderm Development) inactivation in the postnatal heart (Eed CKO ) caused lethal dilated cardiomyopathy. Surprisingly, gene upregulation in Eed CKO was not coupled with loss of H3K27me3. Rather, the activating histone mark H3K27ac increased. EED interacted with histone deacetylases (HDACs) and enhanced their catalytic activity. HDAC overexpression normalized Eed CKO heart function and expression of derepressed genes. Our results uncovered a non-canonical, H3K27me3-independent EED repressive mechanism that is essential for normal heart function. Our results further illustrate that organ dysfunction due to epigenetic dysregulation can be corrected by epigenetic rewiring.

Publication Title

EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE20992
Systematic analysis of miRNA transcriptome of skeletal muscle identifies novel miRNAs and differentially expressed miRNAs in divergent skeletal muscle growth rates of broiler and layer chickens
  • organism-icon Gallus gallus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer, Affymetrix Chicken Genome Array (chicken)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A systematic analysis of the skeletal muscle miRNA transcriptome of chicken varieties with divergent skeletal muscle growth identifies novel miRNAs and differentially expressed miRNAs.

Sample Metadata Fields

Specimen part

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accession-icon GSE20990
Systematic identification of genes involved in embyonic chicken muscle development
  • organism-icon Gallus gallus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer, Affymetrix Chicken Genome Array (chicken)

Description

The genetic closeness and divergent muscle growth rates of broilers and layers make them great models for myogenesis study. In order to discover the molecular mechanisms determining the divergent muscle growth rates and muscle fiber sizes in different chicken lines, we systematically identified differentially expressed genes between broilers and layers during muscle development (embyonic day 10, 12, 14 and 18) by microarray hybridization experiment.

Publication Title

A systematic analysis of the skeletal muscle miRNA transcriptome of chicken varieties with divergent skeletal muscle growth identifies novel miRNAs and differentially expressed miRNAs.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE3013
Actions of tamoxifen in the uterus and its molecular effectors in endometrial carcinogenesis.
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95A Array (hgu95a)

Description

The molecular explanation for tamoxifen serving as a breast cancer treatment but displaying partial estrogenic in the uterus is not known. Previously, we reported that differential promoter context and cofactor recruitment contribute to the tissue specificity of tamoxifen. Here, we investigated the genomic basis for the partial oestrogenic activity of tamoxifen in the endometrium. We showed that tamoxifen not only affects the rate of transcription of oestrogen target genes but also targets a unique set of genes. Since oestrogen and tamoxifen are both able to bind to oestrogen receptors (ERs) and because both promote endometrial carcinogenesis, we hypothesized that the molecular effectors for ERs in endometrial carcinogenesis most likely reside in genes that are commonly targeted by oestrogen and tamoxifen. Among those target genes, we identified a paired-box gene PAX2 that is critically involved in cell proliferation and carcinogenesis in the endometrium. Our experiments also demonstrated that PAX2 is activated by oestrogen and tamoxifen in endometrial carcinomas but not in normal endometrium, and this activation is associated with cancer-linked hypomethylation of the PAX2 promoter.

Publication Title

Hypomethylation-linked activation of PAX2 mediates tamoxifen-stimulated endometrial carcinogenesis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE73677
Transcriptional repression by non-canonical EED stimulation of histone deacetylase activity is required for heart maturation independently of H3K27me3 [Microarray]
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Through H3K27me3 and H3K27ac ChIP-seq and microarray data in wile-tpye (WT) and EED-knockout (CKO) mouse cardiomyocytes, we unexpectedly uncovered a novel mechanism of PRC2-mediated gene repression. EED inactivation in the postnatal heart (EEDCKO) caused progressive, lethal dilated cardiomyopathy, with upregulation of components of the slow-twitch muscle gene program. Surprisingly, upregulation of these genes was not associated with their loss of H3K27me3, but rather with their gain of H3K27 acetylation (H3K27ac), an activating histone mark4,5. Moreover, re-expression of EED in juvenile hearts rescued heart function and normalized H3K27ac, but not H3K27me3.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

View Samples
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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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