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accession-icon GSE42641
A Top-down Systems Analysis Identifies an Innate Feed-forward Inflammatory Circuit Leading to Lethal Influenza Infection
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A systems analysis identifies a feedforward inflammatory circuit leading to lethal influenza infection.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE42639
Transcriptomic comparison of 5 cell types during lethal and non-lethal influenza infection
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Transcriptomic comparison of 5 cell types during lethal and non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity during lethal influenza infection.

Publication Title

A systems analysis identifies a feedforward inflammatory circuit leading to lethal influenza infection.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE28750
Development and Validation of a Novel Molecular Biomarker Diagnostic Test for the Early Detection of Sepsis
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Introduction: Sepsis is a complex immunological response to infection characterized by early hyperinflammation followed by severe and protracted immunosuppression, suggesting that a multi-marker approach has the greatest clinical utility for early detection, within a clinical environment focused on SIRS differentiation. Pre-clinical research using an equine sepsis model identified a panel of gene expression biomarkers that define the early aberrant immune activation. Thus, the primary objective was to apply these gene expression biomarkers to distinguish patients with sepsis from those who had undergone major open surgery and had clinical outcomes consistent with systemic inflammation due to physical trauma and wound healing.

Publication Title

Development and validation of a novel molecular biomarker diagnostic test for the early detection of sepsis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE40715
Gene signature of adult mammary stem cells and mammary cancer stem cells
  • organism-icon Mus musculus
  • sample-icon 24 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

Cancer stemness in Wnt-driven mammary tumorigenesis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE40702
Gene signature of adult mammary stem cells and mammary cancer stem cells (Affymetrix)
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The Wnt/beta-catenin signalling pathway plays a central role in mammary stem cell homeostasis and in breast cancer. We employed the CD29hiCD24+ cell surface antigens to identify a subpopulation of mammary CSCs from Apc1572T/+, a mouse model for metaplastic breast adenocarcinoma, a subtype of triple-negative breast cancer in man. The MaCSCs are capable of recapitulating tumorigenesis when transplanted at low multiplicities in vivo, and of forming self-renewing organoids in vitro. Expression profiling of the different subpopulations sorted from normal and neoplastic mammary tissues revealed that the normal stem cell compartment is more similar to tumor cells than to their own differentiated progenies. Accordingly, Wnt signaling was found to be activated in the subpopulation encompassing normal mammary stem cells, though to a lesser degree than in the tumor cells. By comparing normal with cancer mouse mammary compartments, we were able to derive a MaCSC-specific signature composed of human orthologous genes able to predict poor survival, relapse and distant metastasis in human breast cancer. Finally, upon intravenous injection, only MaCSCs among the different tumor cell subpopulations are able to form metastatic lesions in a broad spectrum of anatomical sites. Overall, our data indicate that constitutive Wnt signaling activation interferes with mammary stem cell homeostasis leading to metaplasia and basal-like adenocarcinomas.

Publication Title

Cancer stemness in Wnt-driven mammary tumorigenesis.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP174500
Role of p110a subunit of PI3-kinase in skeletal muscle mitochondria
  • organism-icon Mus musculus
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Skeletal muscle insulin resistance, decreased phosphatidylinositol 3-kinase (PI3K) activation and altered mitochondrial function are hallmarks of type 2 diabetes. We created mice with a muscle-specific knockout of p110a or p110ß, the two major catalytic subunits of PI3K. We find that mice with muscle-specific knockout of p110a, but not p110ß, display impaired muscle insulin signaling and reduced muscle size due to enhanced proteasomal and autophagic activity. Despite insulin resistance and muscle atrophy, M-p110aKO mice show decreased serum myostatin, increased mitochondrial mass, increased mitochondrial fusion visualized by intravital microscopy, and increased PGC1a expression, especially PCG1a2 and PCG1a3. This leads to enhanced mitochondrial oxidative capacity, striking increases in muscle NADH content, and higher muscle free radical release measured in vivo using pMitoTimer reporter. Thus, p110a is the dominant catalytic isoform of PI3K in muscle in control of insulin sensitivity and muscle mass, and has a unique role in mitochondrial homeostasis in skeletal muscle. Overall design: All studies were performed in male mice on C57BL/6J background. Muscle-specific p110alpha or p11beta knockout mice were generated by crossing mice carrying the Cre recombinase gene driven by the human alpha-skeletal actin (HSA) promoter (Jackson Laboratories Stock Number: 006149) with mice carrying either floxed p110alpha or p110beta alleles in which exon 1 of p110alpha or exon 2 of p110bet was flanked with loxP sites. Skeletal muscle from 2-3-month-old male mice was harvested and RNA was extracted using Trizol. Gene expression profiling was performed using NEBNext mRNA Sample Prep Master Mix kit (NEB) by BioPolymers Facility at Harvard Medical School. Reads were aligned to the mouse genome (GRCm38) using STAR aligner and counted with Subread featureCounts.

Publication Title

Role of p110a subunit of PI3-kinase in skeletal muscle mitochondrial homeostasis and metabolism.

Sample Metadata Fields

Sex, Cell line, Treatment, Subject

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accession-icon GSE70216
Differential gene expression to VEGF in aorta from wild-type and C17S PKARI knock-in mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Angiogenesis is essential for tissue development, wound healing and tissue perfusion, with its dysregulation linked-to tumorigenesis, rheumatoid arthritis and heart disease. Here we show pro-angiogenic stimuli couple to NADPH oxidase-dependent generation of oxidants that catalyse an activating intermolecular-disulphide between regulatory-RI subunits of protein kinase A (PKA), which stimulates PKA-dependent ERK signalling. This is crucial to blood vessel growth as 'redox-dead' Cys17Ser RI knock-in mice fully resistant to PKA disulphide-activation have deficient angiogenesis in models of hind limb ischaemia and tumour-implant growth. Disulphide-activation of PKA represents a new therapeutic target in diseases with aberrant angiogenesis.

Publication Title

Deficient angiogenesis in redox-dead Cys17Ser PKARIα knock-in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE55170
Infection of Myeloid Angiogenic Cells (MACs) with Bartonella henselae (B.h.) induces a chord formation phenotype in vitro.
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Myeloid Angiogenic Cells (MACs) were infected with the intracellular, bacterial pathogen Bartonella henselae (B.h.). Infected cells were seeded onto Matrigel coated plates. While uninfected cells showed no phenotypic changes and died over time, infected cells showed strong phenotypic changes and developed into complex 2D chord networks over the course of long term culture (eg 49d). To examine the changes in gene expression associated with the development of the B.h.dependent chord formation phenotype, RNA was isolated from MACs shortly after isolation (d4) and from cells of the chord structures (+B.h. Matrigel). As primary endothelial cells are also know to form chord networks when cultured on Matrigel, a sample of human umbilical vein endothelial cells (HUVECs) cultured on Matrigel for 12hr was also included in the analysis as a control.

Publication Title

Reprogramming of myeloid angiogenic cells by Bartonella henselae leads to microenvironmental regulation of pathological angiogenesis.

Sample Metadata Fields

Specimen part, Subject, Time

View Samples
accession-icon SRP071739
Changes in RNA expression in human oral cavity carcinoma cells as a result of LDB1 reduction
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

The study was designed to identify differential expressed genes between human oral cavity carcinoma cell lines with and without LDBI knockout Overall design: Three parental human oral cavity carcinoma cell lines were used as control, LDB1 was knocked out in the three parent cell lines to create KO cell lines.

Publication Title

LIM-Only Protein 4 (LMO4) and LIM Domain Binding Protein 1 (LDB1) Promote Growth and Metastasis of Human Head and Neck Cancer (LMO4 and LDB1 in Head and Neck Cancer).

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE32937
MicroRNA-29 in Aortic Dilation: Implications for Aneurysm Formation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We compared the aorta of 6-weeks-old mice (young) with 18-months-old mice (old). Using the publicly available tools Sylamer and DIANA-mirExTra, we identified an enrichment for miR-29 binding sites in the 3'UTR of genes downregulated in the aged aortas. We subsequently showed that inhibition of miR-29 in aged mice prevented dilation of the aorta.

Publication Title

MicroRNA-29 in aortic dilation: implications for aneurysm formation.

Sample Metadata Fields

Age, 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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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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