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accession-icon GSE39881
Lgr5+ve stem cells in nephrogenesis
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Multipotent stem cells and their lineage-restricted progeny drive nephron formation within the developing kidney. Validated markers of these early stem/progenitor populations are essential for deciphering their in vivo function and for evaluating their clinical potential for treating adult kidney disease. Here, we document expression of the adult stem cell marker Lgr5 in the developing kidney and assess the stem/progenitor identity of Lgr5+ve cells via in vivo lineage tracing. The appearance and localization of Lgr5+ve cells coincided with that of the S-shaped body around E14. Lgr5 expression remained restricted to cell clusters within developing nephrons in the cortex until P7, when expression was permanently silenced. In vivo lineage tracing identified Lgr5 as a marker of a novel progenitor population within nascent nephrons dedicated to generating the thick ascending limb of Henle's loop and distal convoluted tubule. The Lgr5 surface marker and experimental models described here will be invaluable for deciphering the contribution of early nephron stem cells to developmental defects and for isolating human nephron progenitors as a prerequisite to evaluating their therapeutic potential.

Publication Title

Lgr5(+ve) stem/progenitor cells contribute to nephron formation during kidney development.

Sample Metadata Fields

Specimen part

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accession-icon SRP107747
Specific labeling of stem cell activity in human colorectal organoids using an ASCL2-responsive minigene
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Organoid technology provides the possibility to culture human colon tissue and patient-derived colorectal cancers (CRC) while maintaining all functional and phenotypic characteristics. Labeling of human colon stem cells (CoSCs), especially in normal and benign tumor organoids, is challenging and therefore limits usability of multi-patient organoid libraries for CoSC research. Here, we developed STAR (STem cell Ascl2 Reporter), a minimal enhancer/promoter element that reports transcriptional activity of ASCL2, a master regulator of LGR5+ CoSC fate. Among others via lentiviral infection, STAR minigene labels stem cells in normal as well as in multiple engineered and patient-derived CRC organoids of different stage and genetic make-up. STAR revealed that stem cell driven differentiation hierarchies and the capacity of cell fate plasticity (de-differentiation) are present at all stages of human CRC development. The flexible and user-friendly nature of STAR applications in combination with organoid technology will facilitate basic research on human adult stem cell biology. Overall design: Cells from different colon organoid types were FACS sorted for stem STemness Ascl2 Reporter activity for transcriptome profiling by RNA-seq.

Publication Title

Specific Labeling of Stem Cell Activity in Human Colorectal Organoids Using an ASCL2-Responsive Minigene.

Sample Metadata Fields

Subject

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accession-icon GSE38964
Identification of eight candidate target genes of the prognsotic 3p loss in cervical cancer by integrative genomic profiling
  • organism-icon Homo sapiens
  • sample-icon 151 Downloadable Samples
  • Technology Badge IconIllumina HumanWG-6 v3.0 expression beadchip

Description

We performed integrative gene dosage and expression profiling to identify candidate target genes of the prognostic 3p loss in cervical cancer.

Publication Title

Identification of eight candidate target genes of the recurrent 3p12-p14 loss in cervical cancer by integrative genomic profiling.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE43974
Pathways for intervention to optimize donor organ quality uncovered: a genome wide gene expression study
  • organism-icon Homo sapiens
  • sample-icon 554 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Background: Strategies to improve long term renal allograft survival have been directed to recipient dependent mechanisms of renal allograft injury. In contrast, no such efforts have been made to optimize organ quality in the donor. In order to get insight into the deleterious gene pathways expressed at different time points during deceased kidney transplantation, transcriptomics was performed on kidney biopsies from a large cohort of deceased kidney transplants.

Publication Title

Hypoxia and Complement-and-Coagulation Pathways in the Deceased Organ Donor as the Major Target for Intervention to Improve Renal Allograft Outcome.

Sample Metadata Fields

Specimen part

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accession-icon GSE85921
APOL1 renal-risk variants induce mitochondrial dysfunction
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

<i>APOL1</i> Renal-Risk Variants Induce Mitochondrial Dysfunction.

Sample Metadata Fields

Specimen part

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accession-icon GSE85920
APOL1 renal-risk variants induce mitochondrial dysfunction (Affymetrix 2)
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Illumina HumanHT-12 V4.0 expression beadchip

Description

To assess differential gene expression by APOL1 renal-risk (2 risk alleles) vs. non-risk (G0G0) genotypes in primary proximal tubule cells (PTCs), global gene expression (mRNA) levels were examined on Affymetrix HTA 2.0 arrays in primary PTCs cultured from non-diseased kidney in African Americans without CKD who underwent nephrectomy for localized renal cell carcinoma.

Publication Title

<i>APOL1</i> Renal-Risk Variants Induce Mitochondrial Dysfunction.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE85919
APOL1 renal-risk variants induce mitochondrial dysfunction (Affymetrix 1)
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Illumina HumanHT-12 V4.0 expression beadchip

Description

To elucidate pathways whereby apolipoprotein L1 gene (APOL1) G1 and G2 variants facilitate kidney disease in African Americans, human embryonic kidney cells (HEK293) were used to establish doxycycline-inducible (Tet-on) cell lines stably expressing reference APOL1 G0 and its G1 and G2 renal-risk variants. Illumina human HT-12-v4 arrays and Affymetrix HTA 2.0 arrays were employed to generate global gene expression data with doxycycline induction. Significantly altered pathways identified through bioinformatics involved mitochondrial function; results were validated using immunoblotting, immunofluorescence and functional assays.

Publication Title

<i>APOL1</i> Renal-Risk Variants Induce Mitochondrial Dysfunction.

Sample Metadata Fields

Specimen part

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accession-icon GSE44722
Transcriptional specialization of human dendritic cell subsets in response to microbial vaccines
  • organism-icon Homo sapiens
  • sample-icon 351 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Illumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Transcriptional specialization of human dendritic cell subsets in response to microbial vaccines.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE44721
IL4 DCs and monocytes stimulated by 13 human vaccines and LPS for 6hr
  • organism-icon Homo sapiens
  • sample-icon 128 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

While dendritic cells (DCs) are known to play a major role in the process of vaccination, the mechanisms by which vaccines induce protective immunity in humans remain elusive. Herein, we used gene microarrays to characterize the transcriptional programs induced over time in human monocyte-derived DCs (moDCs) in vitro in response to influenza H1N1 Brisbane, Salmonella enterica and Staphylococcus aureus. We built a data-driven modular analytical framework focused on 204 pathogen-induced gene clusters. The expression of these modules was analyzed in response to 16 well-defined ligands, targeting TLRs, cytoplasmic PAMP receptors and cytokine receptors. This multi-dimensional framework covers the major biological functions of APC, including the IFN response, inflammation, DC maturation, T cell activation, antigen processing, cell motility and histone regulation. This framework was used to characterize the response of monocytes and moDCs to 14 commercially available vaccines. These vaccines displayed quantitatively and qualitatively distinct modular signatures in monocytes and DCs, in particular Fluzone and Pneumovax, highlighting the functional and phenotypic differences between APC subsets. This modular framework allows the application of systems immunology approaches to study early transcriptional changes in human APC subsets in response to pathogens and vaccines, which might guide the development of improved vaccines.

Publication Title

Transcriptional specialization of human dendritic cell subsets in response to microbial vaccines.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon GSE44720
IFNa DCs and IL4 DCs exposed to H1N1, heat killed S. aureus, or heat killed S. enterica (HKSE) for 1h, 2h, 6h, 12h, or 24h
  • organism-icon Homo sapiens
  • sample-icon 120 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

While dendritic cells (DCs) are known to play a major role in the process of vaccination, the mechanisms by which vaccines induce protective immunity in humans remain elusive. Herein, we used gene microarrays to characterize the transcriptional programs induced over time in human monocyte-derived DCs (moDCs) in vitro in response to influenza H1N1 Brisbane, Salmonella enterica and Staphylococcus aureus. We built a data-driven modular analytical framework focused on 204 pathogen-induced gene clusters. The expression of these modules was analyzed in response to 16 well-defined ligands, targeting TLRs, cytoplasmic PAMP receptors and cytokine receptors. This multi-dimensional framework covers the major biological functions of APC, including the IFN response, inflammation, DC maturation, T cell activation, antigen processing, cell motility and histone regulation. This framework was used to characterize the response of monocytes and moDCs to 14 commercially available vaccines. These vaccines displayed quantitatively and qualitatively distinct modular signatures in monocytes and DCs, in particular Fluzone and Pneumovax, highlighting the functional and phenotypic differences between APC subsets. This modular framework allows the application of systems immunology approaches to study early transcriptional changes in human APC subsets in response to pathogens and vaccines, which might guide the development of improved vaccines.

Publication Title

Transcriptional specialization of human dendritic cell subsets in response to microbial vaccines.

Sample Metadata Fields

Specimen part, Subject, Time

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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