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accession-icon GSE54536
Involvement of endocytosis and alternative splicing in the formation of the pathological process in Parkinson's Disease
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

We performed a whole-transcriptome analysis of the peripheral blood of untreated patients with stage 1 PD (HoehnYahr scale).

Publication Title

Involvement of endocytosis and alternative splicing in the formation of the pathological process in the early stages of Parkinson's disease.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE77558
Analysis of differentially expressed genes between Huntingtons disease and control iPSCs derived GABA MS-like neurons
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Huntingtons disease (HD) is an incurable hereditary neurodegenerative disorder, which manifests itself as a loss of GABAergic medium spiny (GABA MS) neurons in the striatum and caused by an expansion of the CAG repeat in exon 1 of the huntingtin gene. There is no cure for HD, existing pharmaceutical can only relieve its symptoms. Here, induced pluripotent stem cells were established from patients with low CAG repeat expansion in the huntingtin gene, and were then efficiently differentiated into GABA MS-like neurons under defined culture conditions. Analysis of differentially expressed genes between Huntingtons disease and wild type iPSCs derived GABA MS-like neurons has been performed.

Publication Title

Manifestation of Huntington's disease pathology in human induced pluripotent stem cell-derived neurons.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE5679
Comparative gene expression profile of PPARg and RARa ligand treated human dendritic cells
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Our data indicated that activation of the PPARg nuclear receptor induces a retinoid response in human dendritic cells. In order to assess the contribution of retinoid signaling to the PPARg response we decided to use a combination of pharmacological activators and inhibitors of these pathways. Cells were treated with the synthetic PPARg ligand rosiglitazone (RSG), or with RSG along with the RARa antagonist (AGN193109) to block RARa mediated gene expression, or the RARa specific agonists (AM580) alone. This design allows one to determine if retinoid signaling is a downstream event of PPARg activation and what portion of PPARg regulated genes are regulated via induced retinoid signaling.

Publication Title

PPARgamma controls CD1d expression by turning on retinoic acid synthesis in developing human dendritic cells.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE56704
Densely Ionizing Radiation Effects on the Microenvironment Promote Aggressive Trp53 Null Mammary Carcinomas
  • organism-icon Mus musculus
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Densely ionizing radiation is a major component of the space radiation environment and has potentially greater carcinogenic effect compared to sparsely ionizing radiation that is prevalent in the terrestrial environment. It is unknown to what extent the irradiated microenvironment contributes to the differential carcinogenic potential of densely ionizing radiation. To address this gap, 10-week old BALB/c mice were irradiated with 100 cGy sparsely ionizing g-radiation or 10, 30, or 80 cGy of densely ionizing, 350 MeV/amu Si particles and transplanted 3 days later with syngeneic Trp53 null mammary fragments. Tumor appearance was monitored for 600 days. Tumors arising in Si-particle irradiated mice had a shorter median time to appearance, grew faster and were more likely to metastasize. Most tumors arising in sham-irradiated mice were ER-positive, pseudo-glandular and contained both basal keratin 14 and luminal keratin 8/18 cells (designated K14/18), while most tumors arising in irradiated hosts were K8/18 positive (designated K18) and ER negative. Comparison of K18 vs K14/18 tumor expression profiles showed that genes increased in K18 tumors were associated with ERBB2 and KRAS while decreased genes overlapped with those down regulated in metastasis and by loss of E-cadherin. Consistent with this, K18 tumors grew faster than K14/18 tumors and more mice with K18 tumors developed lung metastases compared to mice with K14/18 tumors. However, K18 tumors arising in Si-particle irradiated mice grew even faster and were more metastatic compared to control mice. A K18 Si-irradiated host profile was enriched in genes involved in mammary stem cells, stroma, and Notch signaling. Thus systemic responses to densely ionizing radiation enriches for a ER-negative, K18-positive tumor, whose biology is more aggressive compared to similar tumors arising in non-irradiated hosts.

Publication Title

Densely ionizing radiation acts via the microenvironment to promote aggressive Trp53-null mammary carcinomas.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP065865
Gene Networks and Blood Biomarkers of Methamphetamine-Associated Psychosis: A Preliminary Integrative RNA-Sequencing Report
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The clinical presentation, course and treatment of methamphetamine-associated psychosis (MAP) are similar to that observed in schizophrenia (SCZ) and subsequently MAP has been hypothesized as a pharmacological and environmental model of SCZ. However, several challenges currently exist in accurately diagnosing MAP at the molecular and neurocognitive level before the MAP model can contribute to the discovery of SCZ biomarkers. We directly assessed subcortical brain structural volumes and clinical parameters of MAP within the framework of an integrative genome-wide RNA-Seq blood transcriptome analysis of subjects diagnosed with MAP (N=10), METH-dependency without psychosis (MA) (N=10) and healthy controls (N=10). We used RNA-Sequencing gene expression to characterize molecular signatures associated to METH and MAP status compared to healthy control subjects. Overall design: Peripheral blood luekocytes gene expression was subject to transcriptional analysis for 10 MAP subjects, 10 subjects with METH-dependency without psychotic symptomics and 10 healthy controls.

Publication Title

Candidate gene networks and blood biomarkers of methamphetamine-associated psychosis: an integrative RNA-sequencing report.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE48280
Expression data from inflammatory myopathies
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

MHC-I overexpression in muscle biopsies is a hallmark of inflammatory myopathies.However the mechanisms of MHC-I overexpression in each disease is not well understood. Microarray analysis from MHC-I-microdissected myofibers showed a differential expression signature in each inflammatory myopathy. Innate immunity and IFN-I pathways are upregulated vs healthy controls, specifically in dermatomyositis (DM).

Publication Title

Altered RIG-I/DDX58-mediated innate immunity in dermatomyositis.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE48392
Response of mammary tissue to high-LET HZE particle (Silicon ions) radiation or low-LET gamma-rays
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.1 ST Array (mogene11st)

Description

Transcriptional profiling of mammary tissue irradiated at 10 weeks of age with either 100 cGy sparsely ionizing gamma-rays, or 10 cGy or 30 cGy densely ionizing radiation (350 MeV/amu Si). Mammary tissue was collected 1 weeks, 4 weeks, and 12 weeks post-irradiation.

Publication Title

Irradiation of juvenile, but not adult, mammary gland increases stem cell self-renewal and estrogen receptor negative tumors.

Sample Metadata Fields

Sex, Specimen part, Time

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accession-icon SRP150459
Transcriptional profiling by 4SU-seq in mouse ESCs and ESC-derived neural progenitor cells.
  • organism-icon Mus musculus
  • sample-icon 31 Downloadable Samples
  • Technology Badge IconNextSeq 550

Description

Nascent RNA was metabolically labelled with 4SU in undifferentiated and ESC-derived neural progenitor cells (NPCs). 4SU incorporated RNA was isolated and deep-sequenced at day 0 (ESCs), 3, 5 and 7 of differentiation. NPC differentiation was monitored through expression of a GFP reporter insereted into the Sox1 locus (46C reporter ESC line; PMID: 12524553). The aim was to monitor changes in transcription as ESCs differentiate into NPCs and relate this to enhancer activity. Overall design: For each of the 4 differentiation time points, two independent biological replicates were prepared and sequenced. For each assayed time point, both merged and individual replicate 4SU-seq profiles were generated.

Publication Title

Decreased Enhancer-Promoter Proximity Accompanying Enhancer Activation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE90628
Expression data from human infant kidney derived-CD133+GFP+ and CD133-GFP+
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Previous studies have suggested that CD133+ cells isolated from human kidney biopsies have the potential to ameliorate injury following intravenous (IV) administration in rodent models of kidney disease by integrating into damaged renal tissue and generating specialised renal cells. However, whether renal engraftment of CD133+ cells is prerequisite for ameliorating injury has not yet been unequivocally resolved. Here, we have established a cisplatin-induced nephropathy model in immunodeficient rats to assess the efficacy of CD133+ human kidney cells in restoring renal health, and to determine the fate of these cells after systemic administration. Specifically, following IV administration, we evaluated the impact of the CD133+ cells on renal function by undertaking longitudinal measurements of the glomerular filtration rate using a novel transcutaneous device. Furthermore, using histological assays, we assessed whether the human kidney cells could promote renal regeneration, and if this was related to their ability to integrate into the damaged kidneys. Our results show that both CD133+ and CD133- cells improve renal function and promote renal regeneration to a similar degree. However, this was not associated with engraftment of the cells into the kidneys. Instead, after IV administration, both cell types were exclusively located in the lungs, and had disappeared by 24 hours. Our data therefore indicate that renal repair is not mediated by CD133+ cells homing to the kidneys and generating specialised renal cells. Instead, renal repair is likely to be mediated by paracrine or endocrine factors.

Publication Title

Human Kidney-Derived Cells Ameliorate Acute Kidney Injury Without Engrafting into Renal Tissue.

Sample Metadata Fields

Specimen part, Disease stage

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accession-icon GSE32015
Expression data from inducible ES stable cell lines
  • organism-icon Mus musculus
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In order to identify the effects of the induction of the gene of interest on the mouse ES transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the different inducible cell lines

Publication Title

Reverse engineering a mouse embryonic stem cell-specific transcriptional network reveals a new modulator of neuronal differentiation.

Sample Metadata Fields

Specimen part

View Samples

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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