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accession-icon GSE80244
Expression data from the neuron model of Alzheimer's disease (AD)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To delineate the mechanism by which human mitochondrial transcriptional factor A (hTFAM) suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment.

Publication Title

Human mitochondrial transcriptional factor A breaks the mitochondria-mediated vicious cycle in Alzheimer's disease.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE80245
Expression data from the neuron model of Alzheimer's disease (AD) with or without treatment of recombinant human mitochondrial transcriptional factor A (rhTFAM) protein
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To delineate the mechanism by which hTFAM suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment.

Publication Title

Human mitochondrial transcriptional factor A breaks the mitochondria-mediated vicious cycle in Alzheimer's disease.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE80242
Expression data from Alzheimer's disease (AD) model mouse and AD model mouse overexpressing human mitochondrial transcriptional factor A (hTFAM)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To delineate the mechanism underlying the amelioration of AD pathophysiology by hTFAM, we performed gene expression profiling using hippocampal RNAs from the AD model mouse and AD model mouse overexpressing human TFAM.

Publication Title

Human mitochondrial transcriptional factor A breaks the mitochondria-mediated vicious cycle in Alzheimer's disease.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE36980
Expression data from post mortem Alzheimer's disease brains
  • organism-icon Homo sapiens
  • sample-icon 78 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD)

Publication Title

Altered expression of diabetes-related genes in Alzheimer's disease brains: the Hisayama study.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE36981
Expression data from Alzheimer's disease model mouse
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD)

Publication Title

Altered expression of diabetes-related genes in Alzheimer's disease brains: the Hisayama study.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon SRP076671
Transcriptome analysis of mouse IgG1 memory B cell subsets
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

IgE plays an essential role in the pathogenesis of allergies and its production is strongly regulated. A transient IgE germinal center phase and lack of IgE memory cells limit the generation of pathogenic IgE, but this can be overcome by sequential switching of IgG1 cells to IgE. We investigated which population of IgG1 cells can give rise to IgE-producing cells in memory responses. We identified three populations of IgG1 memory B cells (DP:CD73+CD80+, SP:CD73-CD80+, DN:CD73-CD80-) that generate IgE plasma cells of high or low affinity, but none gives rise to IgE germinal center cells or IgE memory cells. The two memory IgG1 populations differ however in their ability to differentiate into IgG1 plasma cells and germinal center cells, and to expand the IgG1 memory B cell pool. To explore the molecular mechanisms that may explain the distinct functions of IgG1 memory B cell subsets we compared their expression by transcriptome analysis using next generation sequencing. Overall design: mRNA profiles of quadruplicates of double positive (DP:CD73+CD80+), single positive (SP:CD73-CD80+), double negative (DN:CD73-CD80-) IgG1 memory B cells along with IgG1 germinal center (GC) cells and naïve B cells were generated using Illumina high throughput sequencing.

Publication Title

IgG1 memory B cells keep the memory of IgE responses.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE49033
Expression data from IgE+ and IgG1+ B lymphocytes in mice infected with Nippostrongylus brasiliensis
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The mechanisms involved in the maintenance of memory IgE responses are poorly understood, and the role played by germinal center (GC) IgE cells in these memory responses is particularly unclear. IgE B-cell differentiation is characterized by a transient GC phase, a bias towards the plasma cell (PC) fate, and dependence on sequential switching for the production of high-affinity IgE. We show here that IgE GC B cells are unfit to undergo the conventional GC differentiation program due to impaired B-cell receptor function and increased apoptosis. IgE GC cells fail to populate the GC light zone and are unable to contribute to the memory and long-lived PC compartments. Furthermore, we demonstrate that direct and sequential switching are linked to distinct B-cell differentiation fates: direct switching generates IgE GC cells, whereas sequential switching gives rise to IgE plasma cells. We propose a comprehensive model for the generation and memory of IgE responses.

Publication Title

The distinctive germinal center phase of IgE+ B lymphocytes limits their contribution to the classical memory response.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE40488
Treg cells
  • organism-icon Mus musculus
  • sample-icon 8 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

Neuropilin 1 is expressed on thymus-derived natural regulatory T cells, but not mucosa-generated induced Foxp3+ T reg cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE40443
iTreg cells compared to WT Total Treg
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

iTreg cells from Tbmc mLN mice treated with one week of 1% Oral Ova were compared to Total Treg from WT mice.

Publication Title

Neuropilin 1 is expressed on thymus-derived natural regulatory T cells, but not mucosa-generated induced Foxp3+ T reg cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE40441
Comparison of Splenic Nrp1- and Nrp1+ Treg Populations
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To compare subpopulations of Treg cells in wild type mice based upon Nrp1 Expression, differentiating nTreg and iTreg

Publication Title

Neuropilin 1 is expressed on thymus-derived natural regulatory T cells, but not mucosa-generated induced Foxp3+ T reg cells.

Sample Metadata Fields

Specimen part

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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