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accession-icon GSE33774
Expression data from gingival tissue
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The experiment aims to identify transcriptional effects differences between periimplantitis, Parodontitis and healthy gingival tissue

Publication Title

Peri-implantitis versus periodontitis: functional differences indicated by transcriptome profiling.

Alternate Accession IDs

E-GEOD-33774

Sample Metadata Fields

Specimen part

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accession-icon GSE18765
The transcriptome of prospectively isolated adult neural stem cells
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Since the discovery of adult neural stem cells, their exact identity is still under discussion. Moreover, the lack of a reproducible procedure to purify neural stem cells prospectively rather than by growing them in vitro has so far precluded their study at the transcriptome level. Here we demonstrate a novel procedure to prospectively isolate neural stem cells from the adult mouse subependymal zone on the basis of their GFAP- and prominin1-expression by fluorescence-activated cell sorting. All self-renewing, multipotent stem cells are contained in this fraction at 70% purity. The stem cell identity of these double-positive cells is further demonstrated in vivo, by using a novel split-Cre-technology for fate mapping.

Publication Title

In vivo fate mapping and expression analysis reveals molecular hallmarks of prospectively isolated adult neural stem cells.

Alternate Accession IDs

E-GEOD-18765

Sample Metadata Fields

Specimen part

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accession-icon GSE58813
Dickkopf 3 Promotes the Differentiation of Substantia Nigra Dopaminergic Neurons In Vivo and from Pluripotent Stem Cells In Vitro
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

WNT1/beta-catenin signaling plays a crucial role in the generation of mesodiencephalic dopaminergic (mdDA) neurons including the Substantia nigra pars compacta (SNc) subpopulation, whose degeneration is a hallmark of Parkinsons Disease (PD). However, the precise functions of WNT/beta-catenin signaling in this context remain unknown. Using mutant mice, primary ventral midbrain (VM) cells and pluripotent stem cells (mouse embryonic stem cells and induced pluripotent stem cells), we show that Dickkopf 3 (DKK3), a secreted glycoprotein that modulates WNT/beta-catenin signaling, is specifically required for the correct differentiation of a rostrolateral mdDA precursor subset into SNc DA neurons.

Publication Title

Dickkopf 3 Promotes the Differentiation of a Rostrolateral Midbrain Dopaminergic Neuronal Subset In Vivo and from Pluripotent Stem Cells In Vitro in the Mouse.

Alternate Accession IDs

E-GEOD-58813

Sample Metadata Fields

Specimen part

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accession-icon SRP182694
Point mutations in the PDX1 transactivation domain impair human ß-cell development and function (RNA-Seq)
  • organism-icon Homo sapiens
  • sample-icon 56 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Missense mutations in coding region of PDX1 predispose to type-2 diabetes mellitus as well as cause MODY through largely unexplored mechanisms. Here, we screened a large cohort of subjects with increased risk for diabetes and identified two subjects with impaired glucose tolerance carrying heterozygous missense mutations in the PDX1 coding region leading to single amino acid exchanges (P33T, C18R) in its transactivation domain. We generated iPSCs from patients with heterozygous PDX1P33T/+, PDX1C18R/+ mutations and engineered isogenic cell lines carrying homozygous PDX1P33T/P33T, PDX1C18R/C18R mutations and a heterozygous PDX1 loss-of-function mutation (PDX1+/-). Using an in vitro ß-cell differentiation protocol, we demonstrated that both PDX1P33T/+, PDX1C18R/+ and PDX1P33T/P33T, PDX1C18R/C18R mutations impair ß-cell differentiation and function. Furthermore, PDX1+/- and PDX1P33T/P33T mutations reduced differentiation efficiency of pancreatic progenitors (PPs), due to downregulation of PDX1-bound genes, including transcription factors MNX1 and PDX1 as well as insulin resistance gene CES1. Additionally, both PDX1P33T/+ and PDX1P33T/P33T mutations in PPs reduced the expression of PDX1-bound genes including the long-noncoding RNA, MEG3 and the imprinted gene NEURONATIN, both involved in insulin synthesis and secretion. Our results reveal mechanistic details of how diabetes-associated PDX1 point mutations impair human pancreatic endocrine lineage formation and ß-cell function and contribute to pre-disposition for diabetes. Overall design: We performed RNA-seq of control and isogenic PDX1 mutant cell lines at PP stage

Publication Title

Point mutations in the PDX1 transactivation domain impair human β-cell development and function.

Alternate Accession IDs

GSE125769

Sample Metadata Fields

Subject

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accession-icon SRP066445
Investigating gene expression changes upon ageing in chm mutants
  • organism-icon Drosophila melanogaster
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1500

Description

We report here mRNA-seq data of adult male Drosophila head tissues. We compare two different ages: young and midlife as well as chm/chameau (CG5229) heterozygous mutants. Overall design: Comparison of ageing effect (young vs. midlife) in wild-type and mutant.

Publication Title

Life span extension by targeting a link between metabolism and histone acetylation in Drosophila.

Alternate Accession IDs

GSE75216

Sample Metadata Fields

Sex, Subject

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accession-icon GSE28014
Identification of genes associated with lens regeneration from the cornea in Xenopus laevis tadpoles
  • organism-icon Xenopus laevis
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Xenopus laevis Genome Array (xenopuslaevis)

Description

Surgical removal of the lens from larval Xenopus laevis results in a rapid transdifferention of central corneal cells to form a new lens. The trigger for this process is understood to be an induction event arising from the unprecedented contact between the cornea and the vitreous humour that occurs following lens removal. The identity of this trigger is unknown. Here, we have used a functional transgenic approach to show that BMP signalling is required for lens regeneration and a microarray approach to identify genes that are upregulated specifically during this process. Analysis of the array data strongly implicates Wnt signalling and Pitx transcription factors in this process. Pluripotency genes, in contrast, are not upregulated, supporting the idea that corneal cells transdifferentiate without returning to a stem cell state. Furthermore, several genes from the array were expressed in the forming lens during embryogenesis. One of these, nipsnap1, is a known direct target of BMP signalling. We suggest that, as with tail regeneration, activation of multiple developmental signalling pathways could drive lens regeneration from the cornea.

Publication Title

Transdifferentiation from cornea to lens in Xenopus laevis depends on BMP signalling and involves upregulation of Wnt signalling.

Alternate Accession IDs

E-GEOD-28014

Sample Metadata Fields

Specimen part

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accession-icon GSE5140
Creatine increases health and life span in mice
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Here we show that oral creatine (Cr) supplementation leads to increased life span in mice. Treated mice showed improved neurobehavioral performance, decreased accumulation of the aging pigment lipofuscin and upregulation of anti-aging genes in brain. As Cr is virtually free of adverse effects, it may be a promising food supplement for healthy aging in man.

Publication Title

Creatine improves health and survival of mice.

Alternate Accession IDs

E-GEOD-5140

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3057
Temporal pattern of gene expression in the late third instar larvae and prepupae of Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

This study identifies genes that alter their expression in synchrony with the late third instar and prepupal pulses of 20E.

Publication Title

The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis.

Alternate Accession IDs

E-GEOD-3057

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE3069
Identification of genes dependent on the Ecdysone receptor (EcR) at the onset of metamorphosis in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

This study identifies those genes that are dependent on EcR for their proper regulation at the onset of metamorphosis in Drosophila melanogaster.

Publication Title

The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis.

Alternate Accession IDs

E-GEOD-3069

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3060
Identification of 20E-regulated genes in Drosophila cultured larval organs
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome Array (drosgenome1)

Description

To identify 20E-regulated genes, wandering third instar larvae were dissected and their organs were cultured in the presence of either no hormone, 20E alone, cycloheximide alone, or 20E plus cycloheximide for six hours.

Publication Title

The genomic response to 20-hydroxyecdysone at the onset of Drosophila metamorphosis.

Alternate Accession IDs

E-GEOD-3060

Sample Metadata Fields

No sample metadata fields

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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