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accession-icon GSE7400
Hematopoietic stem cell mobilization with G-CSF (gene expression profiling)
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Granulocyte-colony stimulating factor (G-CSF) is used to boost granulocyte counts in immunocompromised patients, but its effects on the immune system may be counter productive. We tested the hypothesis that G-CSF mobilized peripheral blood stem cell (PBSC) products are immunologically down regulated based on gene microarray analysis.

Publication Title

Hematopoietic stem cell mobilization with G-CSF induces innate inflammation yet suppresses adaptive immune gene expression as revealed by microarray analysis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7510
Acute graft-versus-host disease (gene expression profiling)
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Allogeneic hematopoietic stem cell transplantation (HSCT) is the treatment of choice for high-risk hematological malignancies, yet a major complication associated with this therapy is acute graft-versus-host disease (GVHD). Despite a well-defined pathophysiological mechanism, there are no definitive markers for predicting acute GVHD development or progression to advanced stages. In the current study, we enrolled four acute GVHD and four acute GVHD-free recipients of allogeneic HSCT and collected peripheral blood just prior to onset of clinical acute GVHD for analysis on Affymetrix GeneChip Human Genome U133 Plus 2.0 microarrays. We noted significant differences in expression of 1,658 genes between control and acute GVHD patients, based on an analysis of covariance (ANCOVA) by type of transplant, a pooled error estimate, and a false discovery rate (FDR) of 10%. In conclusion, we offer the first report of a preliminary molecular signature of acute GVHD in allogeneic HSCT patients.

Publication Title

A preliminary gene expression profile of acute graft-versus-host disease.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP195418
Transcriptome Signature of Cellular Senescence
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000, Illumina HiSeq 2500

Description

Abstract: Cellular senescence, an integral component of aging and cancer, arises in response to diverse triggers, including telomere attrition, macromolecular damage, and signaling from activated oncogenes. At present, senescent cells are identified by the combined presence of multiple traits, such as senescence-associated protein expression and secretion, DNA damage, and ß-galactosidase activity; unfortunately, these traits are neither exclusively nor universally present in senescent cells. To identify robust shared markers of senescence, we have performed RNA-sequencing analysis across 8 diverse models of senescence triggered in human diploid fibroblasts (WI-38, IMR-90) and endothelial cells (HUVEC, HAEC) by replicative exhaustion, exposure to ionizing radiation or doxorubicin, and expression of the oncogene HRASG12V. The intersection of the altered transcriptomes revealed 47 RNAs consistently elevated and 26 RNAs consistently reduced across all senescence models, including many protein-coding mRNAs and some long noncoding RNAs. We propose that these shared transcriptome profiles will enable the identification of senescent cells in vivo, the investigation of their roles in aging and malignancy, and the development of strategies to target senescent cells therapeutically. Overall design: Transcriptomic analysis of various cell line models of senescence and their respective controls

Publication Title

Transcriptome signature of cellular senescence.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE7768
Expression data from spleens of mice immunized using LPS vs MPL as adjuvant.
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

An unresolved issue in immunology is the extent to which inflammatory effects are needed for robust T cell responses. In this study, mice were immunized by iv injection using either high toxicity lipopolysaccharide (LPS) or low toxicity monophosphoryl lipid A (MPL) as adjuvant. Six hours after iv immunization, whole spleens were harvested and gene expression was measured in unfractionated splenic populations of cells. The analysis indicated that the low toxicity adjuvanticity of MPL was associated with TLR4-mediated signaling that was biased to the TRIF branch of TLR4, while LPS generated balanced MyD88 and TRIF-associated outcomes.

Publication Title

The vaccine adjuvant monophosphoryl lipid A as a TRIF-biased agonist of TLR4.

Sample Metadata Fields

No sample metadata fields

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accession-icon E-MEXP-3786
Transcription profiling by array of mouse male retinas to investugate IGF-I-induced chronic gliosis and retinal stress
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death.

Publication Title

Insulin-like Growth Factor 2 Overexpression Induces β-Cell Dysfunction and Increases Beta-cell Susceptibility to Damage.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE37230
c-Myc is a universal amplifier of gene expression
  • organism-icon Mus musculus
  • sample-icon 15 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

c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE37222
c-Myc is a universal amplifier of gene expression [Microarray]
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The c-Myc HLH-bZIP protein has been implicated in physiological or pathological growth, proliferation, apoptosis, metabolism and differentiation at the cellular, tissue or organismal levels via regulation of numerous target genes. In part due to the incomplete inventory and functional accounting of Mycs targets, no principle unifies Myc action. To relate the dynamics of Myc-binding with target expression and function in a system where Myc-levels are temporally and physiologically regulated, the transcriptomes and the genome-wide distributions of Myc, RNA polymerase II and chromatin modifications were compared during lymphocyte activation and in ES cells. A remarkably simple rule emerged from this quantitative analysis: Myc is not an on-off switch, but is a non-linear amplifier of expression, acting universally at active genes, except for immediate early genes that are strongly induced before Myc. This rule of Myc action explains the vast majority of Myc biology observed in literature.

Publication Title

c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP171164
Linking cell dynamics with coexpression networks to characterize key events in chronic virus infections
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The host immune response against an infection requires the coordinated action of many diverse cell subsets that dynamically adapt to the pathogen threat. Here we combined WGCNA and DCQ to analyse time-resolved mouse splenic transcriptomes in acute and chronic LCMV infections. This approach allowed to better characterize the dynamic cell events occurring in complex tissues such as the induction of the adaptive T cell response which requires the coordination of monocytes/macrophages and CD8+ T cells. Overall design: mRNA profiles of CD8 T cells and macrophages (in duplicate days 0 and 7 post-infection) from C57BL/6 mice infected with 2x10E2 pfu of LCMV strain Docile, generated by deep sequencing.

Publication Title

Linking Cell Dynamics With Gene Coexpression Networks to Characterize Key Events in Chronic Virus Infections.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE5281
Alzheimer's disease and the normal aged brain (steph-affy-human-433773)
  • organism-icon Homo sapiens
  • sample-icon 157 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Information about the genes that are preferentially expressed during the course of Alzheimers disease (AD) could improve our understanding of the molecular mechanisms involved in the pathogenesis of this common cause of cognitive impairment in older persons, provide new opportunities in the diagnosis, early detection, and tracking of this disorder, and provide novel targets for the discovery of interventions to treat and prevent this disorder. Information about the genes that are preferentially expressed in relationship to normal neurological aging could provide new information about the molecular mechanisms that are involved in normal age-related cognitive decline and a host of age-related neurological disorders, and they could provide novel targets for the discovery of interventions to mitigate some of these deleterious effects.

Publication Title

Gene expression profiles in anatomically and functionally distinct regions of the normal aged human brain.

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Disease stage, Race

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accession-icon SRP126449
Suppressive and stimulatory host processes during virus infection fate decisions
  • organism-icon Mus musculus
  • sample-icon 32 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The processes and mechanisms of virus infection fate decisions that are the result of a dynamic virus - immune system interaction with either an efficient effector response and virus elimination or an alleviated immune response and chronic infection are poorly understood. Here we characterized the host response to acute and chronic lymphocytic choriomeningitis virus (LCMV) infections by gene coexpression network analysis of time-resolved splenic transcriptomes. We found first, an early attenuation of inflammatory monocyte/macrophage prior to the onset of T cell exhaustion and second, a critical role of the XCL1-XCR1 communication axis during the functional adaptation of the T cell response to the chronic infection state. These findings not only reveal an important feedback mechanism that couples T cell exhaustion with the maintenance of a lower level of effector T cell response but also suggest therapy options to better control virus levels during the chronic infection phase. Overall design: mRNA profiles of spleens (in duplicate, days 0, 3, 5, 6, 7, 9 and 31 post-infection) and macrophages (in triplicate, day 6 post-infection) from C57BL/6 mice infected with 2x10E2 (acute) or 2x10E6 (chronic) pfu of LCMV strain Docile, generated by deep sequencing.

Publication Title

Systems analysis reveals complex biological processes during virus infection fate decisions.

Sample Metadata Fields

No sample metadata fields

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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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