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accession-icon SRP095604
Genome-wide transcriptome profiles in Control and Schizophrenia hiPSC-dervied NPC [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We Report the genome-wide RNA expression levels in control and schizophrenia hiPSC dervied NPC treated with neuronal media for 2 days. In total about 15,000 gene expression were detected in all samples, of which 1349 were dysregualted. Overall design: Examination, identification and comparision of mRNA expression profliles in control and schizophrenia npc

Publication Title

Common developmental genome deprogramming in schizophrenia - Role of Integrative Nuclear FGFR1 Signaling (INFS).

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE473
PGA Human CD4+ Lymphocytes
  • organism-icon Homo sapiens
  • sample-icon 175 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This project is based on the hygiene hypothesis that exposure to TB provides a protective mechanism against asthma through specific cytokines and the balance of Th1, Th2 cells. Additionally, expression changes are examined in patients with and without atopy in combination with asthma and PPD status. Expression levels were evaluated in CD4+ cells isolated from peripheral blood of 30 patients. Each patient was evaluated on the entire U133 Affymetrix GeneChip set.

Publication Title

A module-based analytical strategy to identify novel disease-associated genes shows an inhibitory role for interleukin 7 Receptor in allergic inflammation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE10041
Genomic Counter-Stress Changes Induced by Mind-Body Practice
  • organism-icon Homo sapiens
  • sample-icon 69 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Mind-body practices that elicit the relaxation response (RR) have been used worldwide for millennia to prevent and treat disease. The RR is believed to be the counterpart to stress response and is characterized by decreased oxygen consumption, increased exhaled nitric oxide, and reduced psychological distress. Individuals experiencing chronic psychological stress have the opposite pattern of physiology and a characteristic transcriptional profile. We hypothesized that consistent, long-term practice of RR techniques results in characteristic changes in gene expression. We tested this hypothesis by assessing the transcriptional profile of whole blood in healthy, long-term practitioners of daily RR practice (group M) in comparison to healthy controls (group N1). The signature obtained has been validated on new subject data.

Publication Title

Genomic counter-stress changes induced by the relaxation response.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE6012
Skin biopsies from atopic eczema and healthy controls
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The aim of this study was to find disease-associated genes in atopic eczema.

Publication Title

Increased expression of aquaporin 3 in atopic eczema.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE56483
Modeling the clinical phenotype of BTK inhibition in the mature murine immune system
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Using the novel BTK inhibitor PF-303, we model the clinical phenotype of BTK inhibition by systematically examining the impact of PF-303 on the mature immune system in mice autoimmune indications. However, our current knowledge of the role of BTK in immune competence has been gathered in the context of genetic inactivation of btk in both mice and man. Using the novel BTK inhibitor PF-303, we model the clinical phenotype of BTK inhibition by systematically examining the impact of PF-303 on the mature immune system in mice. We implicate BTK in tonic BCR signaling, demonstrate dependence of the T3 B cell subset and IgM surface expression on BTK activity, and find that B1 cells survive and function independently of BTK. While BTK inhibition does not impact humoral memory survival, antigen-driven clonal expansion of memory B cells and antibody secreting cell generation are inhibited. These data define the role of BTK in the mature immune system and mechanistically predict the clinical phenotype of BTK inhibition.

Publication Title

Modeling the clinical phenotype of BTK inhibition in the mature murine immune system.

Sample Metadata Fields

Specimen part

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accession-icon GSE18477
Normal expression of facial prominences in stage 18 chicken embros
  • organism-icon Gallus gallus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

The face is one of the three regions most frequently affected by congenital defects in humans. In order to understand the molecular mechanisms involved it is necessary to have a more complete picture of gene expression in the embryo. Here we use microarrays to profile expression in chicken facial prominences, post neural crest migration and prior to differentiation of mesenchymal cells. Chip-wide analysis revealed that maxillary and mandibular prominences had similar expression profiles while the frontonasal mass chips were distinct. Of the 3094 genes that were differentially expressed in one or more regions of the face, a group of 56 genes was subsequently validated with quantitative PCR and a subset examined with in situ hybridization. Microarrays trends were consistent with the QPCR data for the majority of genes (81%). On the basis of QPCR and microarray data, groups of genes that characterize each of the facial prominences can be determined.

Publication Title

Whole genome microarray analysis of chicken embryo facial prominences.

Sample Metadata Fields

Specimen part

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accession-icon GSE18574
Allergen-challenged CD4+ cells from patients with seasonal allergic rhinitis
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconSentrix Human-6 Expression BeadChip

Description

Seasonal allergic rhinitis (SAR) is a complex disease that is caused by many interacting genes and environmental factors. It is also an excellent model disease for clinical studies; it is common, it is seasonal, and since it takes place in the nasal cavity it can be studied in vivo non-invasively. Furthermore, the key disease cell, the Th2 cell is known. We study SAR using allergen-challenged CD4+ cells from allergic patients.

Publication Title

Highly interconnected genes in disease-specific networks are enriched for disease-associated polymorphisms.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE38088
Expression data from human induced pluripotent stem cell-derived teratomas and embryoid bodies
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The tumorigenicity of human pluripotent stem cells (hPSCs) is a major safety concern for their application in regenerative medicine. Here we identify the tight-junction protein Claudin-6 as a specific cell surface marker of hPSCs that can be used to selectively remove Claudin-6-positive cells from mixed cultures. We show that Claudin-6 is absent in adult tissues but highly expressed in undifferentiated cells, where it is dispensable for hPSC survival and self-renewal. We use three different strategies to remove Claudin-6-positive cells from mixed populations: an antibody against Claudin-6; a cytotoxin-conjugated antibody that selectively targets undifferentiated cells; and clostridium perfringens enterotoxin, a toxin that binds several Claudins, including Claudin-6, and efficiently kills undifferentiated cells, thus eliminating the tumorigenic potential of hPSC-containing cultures. This work provides a proof of concept for the use of Claudin-6 to eliminate residual undifferentiated hPSCs from culture, highlighting a strategy that may increase the safety of hPSC-based cell therapies.

Publication Title

Immunologic and chemical targeting of the tight-junction protein Claudin-6 eliminates tumorigenic human pluripotent stem cells.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon E-MEXP-104
Transcription profiling of mouse pressure overload induced cardiomyopathy in gp130 knock-out mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Comparison between wild-type and cardiomyocyte-restricted knock-out of IL6 cytokines receptor component gp130 after surgical intervention for pressure-overload induced cardiomyopathy.

Publication Title

Nkx2-5 pathways and congenital heart disease; loss of ventricular myocyte lineage specification leads to progressive cardiomyopathy and complete heart block.

Sample Metadata Fields

Sex, Specimen part, Subject

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accession-icon GSE39916
Expression data from murine bone marrow-resident plasma cells and spleen mature follicular B cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

CD138+ B220- plasma cells were sorted from bone marrow and B220+ CD23+ mature follicular B cells were sorted from the spleens. Plasma cells were sorted from C57BL/6 mice 7 days after boosting with antigen, with mice first primed with an i.p. injection of KLH/IFA followed by boost at day 21 with KLH/PBS i.p. Mature B cells were sorted from antigen-nave C57BL/6 mice.

Publication Title

Heterogeneous nuclear ribonucleoprotein L-like (hnRNPLL) and elongation factor, RNA polymerase II, 2 (ELL2) are regulators of mRNA processing in plasma cells.

Sample Metadata Fields

Specimen part

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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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