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accession-icon GSE75344
Circulating lymphoid committed progenitors after allogeneic stem cell transplantation in humans
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Lymphoid committed CD34+lin-CD10+CD24- progenitors undergo a rebound at month 3 after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in the absence of acute graft-versus-host disease (aGVHD). Here, we analyzed transcriptional programs of cell-sorted circulating lymphoid committed progenitors and CD34+Lin-CD10- non lymphoid progenitors in 11 allo-HSCT patients having (n=5) or not developed (n=6) grade 2 or 3 aGVHD and in 7 age-matched healthy donors. Major deregulated pathways included protein synthesis, energy production, cell cycle regulation and cytoskeleton organization. Notably, genes from protein biogenesis, translation machinery and cell cycle (CDK6) were over-expressed in progenitors from patients in the absence of aGVHD compared with healthy donors and patients affected by aGVHD. Expression of many genes from the mitochondrial oxidative phosphorylation metabolic pathway leading to ATP production were more specifically increased in lymphoid committed progenitors in absence of aGVHD. This was also the case for genes involved in cell mobilization such as those regulating Rho GTPases activity. In all, we show that circulating lymphoid committed progenitors undergo profound changes in metabolism favoring cell proliferation, energy production and cell mobilization after allo-HSCT in humans. These mechanisms are abolished in case of aGVHD or its treatment, indicating a persistent cell-intrinsic defect after exit from bone marrow.

Publication Title

Alterations of circulating lymphoid committed progenitor cellular metabolism after allogeneic stem cell transplantation in humans.

Sample Metadata Fields

Disease, Disease stage, Subject

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accession-icon GSE49804
Expression data from dexamethasone treated mouse embryonic neural progenitor/stem cells isolated from wild type C57Bl/6 or caveolin-1 knockout mice
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Neurosphere cultures prepared from E14.5 mouse cerebral cortex at passage 3 were treated for 4 hours with 100 nM dexamethasone

Publication Title

Caveolin-1 regulates genomic action of the glucocorticoid receptor in neural stem cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE37408
Sucrose modulation of the Arabidopsis thaliana guard-cell transcriptome
  • organism-icon Arabidopsis thaliana
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Microarrays were used to evaluate the effect of sucrose on gene expression in guard cells. Strips of Arabidopsis leaves were incubated with sucrose or mannitol or no sugars, then the leaves were freeze dried and guard cells were dissected from the leaf strips and analyzed.

Publication Title

A comparative study of the Arabidopsis thaliana guard-cell transcriptome and its modulation by sucrose.

Sample Metadata Fields

Specimen part

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accession-icon SRP067022
Expression data from dexamethasone treated mouse embryonic hypothalamic progenitor/stem cells isolated from wild type C57Bl/6 male or female mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We used RNA-Seq to detail the global program of sexually dimorphic dexamethasone regulated gene expression in embryonic hypothalamic neural progenitor/stem cells. Overall design: RNAseq on Primary E14.5 mouse hyothalamic neurosphere cultures. 4 conditions - Male Dex, Male EtOH, Female Dex and Female EtOH. There are 3 biological replicates for each condition and all the 12 samples are run on two lanes (techinical duplicates).

Publication Title

Research Resource: The Dexamethasone Transcriptome in Hypothalamic Embryonic Neural Stem Cells.

Sample Metadata Fields

Sex, Cell line, Treatment, Subject

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accession-icon GSE57386
Gene expression of biopsies, CD14+ and CD14- cells from RA, PsA and PsO patients with Infliximab treatment
  • organism-icon Homo sapiens
  • sample-icon 251 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Divergent gene activation in peripheral blood and tissues of patients with rheumatoid arthritis, psoriatic arthritis and psoriasis following infliximab therapy.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Time

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accession-icon GSE57383
Gene expression of CD14+ cells from RA, PsA and PsO patients with Infliximab treatment
  • organism-icon Homo sapiens
  • sample-icon 111 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

objection: The immune inflammatory disorders rheumatoid arthritis (RA), psoriatic arthritis (PsA) and psoriasis (Ps) share common pathologic features and show responsiveness to anti-tumor necrosis factor (TNF) agents yet they are phenotypically distinct. The aim of this study was to examine if anti-TNF therapy is associated with divergent gene expression profiles in circulating cells and target tissues of patients with these diseases

Publication Title

Divergent gene activation in peripheral blood and tissues of patients with rheumatoid arthritis, psoriatic arthritis and psoriasis following infliximab therapy.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Time

View Samples
accession-icon GSE57405
Gene expression of CD14- cells from RA, PsA and PsO patients with Infliximab treatment
  • organism-icon Homo sapiens
  • sample-icon 109 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

objection: The immune inflammatory disorders rheumatoid arthritis (RA), psoriatic arthritis (PsA) and psoriasis (Ps) share common pathologic features and show responsiveness to anti-tumor necrosis factor (TNF) agents yet they are phenotypically distinct. The aim of this study was to examine if anti-TNF therapy is associated with divergent gene expression profiles in circulating cells and target tissues of patients with these diseases

Publication Title

Divergent gene activation in peripheral blood and tissues of patients with rheumatoid arthritis, psoriatic arthritis and psoriasis following infliximab therapy.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Time

View Samples
accession-icon GSE57376
Synovial biopsies from RA and PsA patients and skin biopsies from Psoriasis patients under Infliximab treatment
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Object: to understand Infliximab treatment effect on the molecular expression of tissue at disease site

Publication Title

Divergent gene activation in peripheral blood and tissues of patients with rheumatoid arthritis, psoriatic arthritis and psoriasis following infliximab therapy.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Time

View Samples
accession-icon SRP058181
mRNA-Seq expression and MS3 proteomics profiling of human post-mortem BA9 brain tissue for Parkinson Disease and neurologically normal individuals
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Parkinson disease (PD) is a neurodegenerative disease characterized by the accumulation of alpha-synuclein (SNCA) and other proteins in aggregates termed “Lewy Bodies” within neurons. PD has both genetic and environmental risk factors, and while processes leading to aberrant protein aggregation are unknown, past work points to abnormal levels of SNCA and other proteins. Although several genome-wide studies have been performed for PD, these have focused on DNA sequence variants by genome-wide association studies (GWAS) and on RNA levels (microarray transcriptomics), while genome-wide proteomics analysis has been lacking. After appropriate filters, proteomics identified 3,558 unique proteins and 283 of these (7.9%) were significantly different between PD and controls (q-value<0.05). RNA-sequencing identified 17,580 protein-coding genes and 1,095 of these (6.2%) were significantly different (FDR p-value<0.05), but only 166 of the FDR significant protein-coding genes (0.94%) were present among the 3,558 proteins characterized. Of these 166, eight genes (4.8%) were significant in both studies, with the same direction of effect. Functional enrichment analysis of the proteomics results strongly supports mitochondrial-related pathways, while comparable analysis of the RNA-sequencing results implicates protein folding pathways and metallothioneins. Ten of the implicated genes or proteins co-localized to GWAS loci. Evidence implicating SNCA was stronger in proteomics than in RNA-sequencing analyses. Notably, differentially expressed protein-coding genes were more likely to not be characterized in the proteomics analysis, which lessens the ability to compare across platforms. Combining multiple genome-wide platforms offers novel insights into the pathological processes responsible for this disease by identifying pathways implicated across methodologies. Overall design: The study consists of mRNA-Seq (29 PD, 44 neurologically normal controls) and three-stage Mass Spectrometry Tandem Mass Tag Proteomics (12 PD, 12 neurologically normal controls) performed in post-mortem BA9 brain tissue. The proteomics samples are a subset of the RNA-Seq samples.

Publication Title

Integrative analyses of proteomics and RNA transcriptomics implicate mitochondrial processes, protein folding pathways and GWAS loci in Parkinson disease.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE21668
Expression data from undifferentiated human embryonic stem cells (hESC) and Day 3.5 mesodermal progenitor (CD326neg CD56+) population
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Our understanding of how mesodermal tissue is formed, has been limited by the absence of specific and reliable markers of early mesoderm commitment. We report that mesoderm commitment from human embryonic stem cells (hESC) is initiated by Epithelial to Mesenchymal transition (EMT) as shown by gene expression profiling and by reciprocal changes in expression of the cell surface proteins, EpCAM/CD326 and NCAM/CD56. Molecular and functional assays reveal that CD326negCD56+ cells, generated from hESC in the presence of activin A, BMP4, VEGF and FGF2, represent a novel, multi-potent mesoderm-committed progenitor population. CD326negCD56+ progenitors are unique in their ability to generate all mesodermal lineages including hematopoietic, endothelial, mesenchymal (bone, cartilage, fat, fibroblast), smooth muscle and cardiomyocytes, while lacking the pluripotency of hESC. CD326negCD56+ cells are the precursors of previously reported, more lineage-restricted mesodermal progenitors. These findings present a novel approach to study how germ layer specification is regulated, and offer a unique target for tissue engineering.

Publication Title

Mapping the first stages of mesoderm commitment during differentiation of human embryonic stem cells.

Sample Metadata Fields

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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