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accession-icon GSE63297
ATAXIN2 is crucial for megakaryocyte protein homeostasis and proper platelet functionality
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Expression of the RNA-binding protein is increased upon megakaryocyte commitment, and may coordinate with mRNA stability and translation during megakaryopoiesis. Reduced expression of ATXN2 in human megakaryocytic cells decreased protein synthesis and total protein content despite equal mRNA expression. Genome-wide comparision of subpolysomal versus polysomal mRNA showed that both protein synthesis and protein degradation are derailed in absence of ATXN2. Furthermore, ATXN2 was associated with PABP and DDX6, proteins that control mRNA stability through the polyA-tail. These findings indicate that ATXN2 is involved in protein metabolism in megakaryocytes and platelet function.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE22656
Expression data from CD71+ cells from the bone marrow of WT, CD70TG, IFNg-/- and CD70TG*IFNg-/- mice.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

CD70TG mice are a model for sterile chronic immune activation and develop Anemia of Inflammation, which is dependent on the production of Ifng by effector CD4 and CD8 T cells.

Publication Title

Chronic IFN-γ production in mice induces anemia by reducing erythrocyte life span and inhibiting erythropoiesis through an IRF-1/PU.1 axis.

Sample Metadata Fields

Specimen part

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accession-icon GSE24892
Nuclear receptors Nur77 and Nurr1 modulate mesenchymal stromal cell migration
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Expression analysis of migrating and non-migrating mesenchymal stromal cells (MSC) in fetal bone marrow

Publication Title

Nuclear receptors Nur77 and Nurr1 modulate mesenchymal stromal cell migration.

Sample Metadata Fields

Specimen part

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accession-icon GSE68374
Differential effects of and on Wnt-signaling in adult and fetal bone marrow-derived MSC
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Expression analysis of adult and fetal derived MSCs

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE81246
Efficient immune responses in immunocompetent individuals developing symptomatic CMV infection
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Primary human cytomegalovirus (HCMV) infection usually goes unnoticed, causing mild or no symptoms in immunocompetent individuals. Some rare severe clinical cases have however been reported without investigation of host immune responses or viral virulence. In this present study, we investigate, for the first time, phenotypic and functional features together with gene expression profiles in immunocompetent adults experiencing a severe primary HCMV infection. Twenty PHIP were enrolled as well as 26 HCMV-seronegative and 39 HCMV-seropositive healthy controls. PHIP had a huge lymphocytosis marked by massive expansion of NK and T cell compartments. Interestingly, PHIP mounted efficient innate and adaptive immune responses with a deep HCMV imprint, revealed mainly by the expansion of NKG2C+ NK cells, CD16+ V2- T cells and conventional HCMV-specific CD8+ T cells. The main effector lymphocytes were activated and displayed an early immune phenotype that developed toward a more mature differentiated status. We suggest that both huge lymphocytosis and excessive lymphocyte activation could contribute to a massive cytokine production known to mediate tissue damage observed in PHIP. Taken together, these findings bring new insights into the comprehensive understanding of immune mechanisms involved during primary HCMV-infection in immunocompetent individuals.

Publication Title

Severe Symptomatic Primary Human Cytomegalovirus Infection despite Effective Innate and Adaptive Immune Responses.

Sample Metadata Fields

Disease

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accession-icon GSE67285
Repression by RB1 characterizes genes involved in the penultimate stage of erythroid differentiation
  • organism-icon Mus musculus
  • sample-icon 61 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE67276
Expression data from murine fetal liver cells, combinations of RB1 family knockouts
  • organism-icon Mus musculus
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Retinoblastoma-1 (RB1), and the RB1-related proteins p107 and p130, reside at a central node in the cell cycle regulatory network. RB1 is required for normal erythroid development in vitro, but is largely dispensable for erythropoiesis in vivo. The modest phenotype caused by RB1 deficiency in mice raises questions about redundancy within the RB1 family, and the role of RB1 in erythroid differentiation. Here we show that RB1 is the major pocket protein that regulates terminal erythroid differentiation. Erythroid cells lacking all pocket proteins exhibit the same cell cycle defects as those deficient for RB1 alone. Further, we show that RB1 broadly represses gene expression in erythroid cells, coincident with the transition from precursor to terminally differentiated cell. RB1-repressed genes are well expressed but downregulated at the final stage of erythroid development. By merging differential and time-dependent changes in expression, we define a group of approximately 800 RB1-repressed genes. As anticipated, these genes are enriched for terms such as cell cycle and DNA metabolic process, but also for terms such as mRNA processing, chromosome organization, and ubiquitin-mediated protein catabolic pro-cess. Our results suggest that RB1-mediated repression of genes involved in noncanonical processes has a central role in terminal erythroid differentiation.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE67278
Expression data from murine fetal liver cells in culture, time course, combinations of RB1 and p107 knockouts
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Retinoblastoma-1 (RB1), and the RB1-related proteins p107 and p130, reside at a central node in the cell cycle regulatory network. RB1 is required for normal erythroid development in vitro, but is largely dispensable for erythropoiesis in vivo. The modest phenotype caused by RB1 deficiency in mice raises questions about redundancy within the RB1 family, and the role of RB1 in erythroid differentiation. Here we show that RB1 is the major pocket protein that regulates terminal erythroid differentiation. Erythroid cells lacking all pocket proteins exhibit the same cell cycle defects as those deficient for RB1 alone. Further, we show that RB1 broadly represses gene expression in erythroid cells, coincident with the transition from precursor to terminally differentiated cell. RB1-repressed genes are well expressed but downregulated at the final stage of erythroid development. By merging differential and time-dependent changes in expression, we define a group of approximately 800 RB1-repressed genes. As anticipated, these genes are enriched for terms such as cell cycle and DNA metabolic process, but also for terms such as mRNA processing, chromosome organization, and ubiquitin-mediated protein catabolic pro-cess. Our results suggest that RB1-mediated repression of genes involved in noncanonical processes has a central role in terminal erythroid differentiation.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon SRP189821
Effect of DR3 agonists on murine Tregs
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

Mice expressing luciferase and GFP under control of the FoxP3 promoter were treated with either the DR3 agonist antibody 4C12 or the DR3 agonist fusion protein TL1A-Ig with low-dose IL-2 (or isotype control antibody), regulatory T cells were sorted from spleens on day 7, and bulk RNA sequencing was performed.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line, Treatment

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accession-icon E-MEXP-70
Transcription profiling by array of human primary CD30+/CD38lo cells differentiating along the megakaryocyte lineage
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

Gene expression profile of primary human CD34+/CD38lo cells differentiating along the megakaryocyte lineage.

Publication Title

Gene expression profile of primary human CD34+CD38lo cells differentiating along the megakaryocyte lineage.

Sample Metadata Fields

Specimen part, Time

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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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