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SRP171164
Mus musculus
8 Downloadable Samples
Illumina 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
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina Genome Analyzer II
Description
BACKGROUND: miRNA have been shown to play an important role during immune-mediated diseases such as inflammatory bowel disease. The aim of this study was to assess differential expression of miRNA between uninfected and infected mice with Clostridium difficile strain VPI 10463 RESULTS: MicroRNA (miRNA)-sequencing analysis indicated that miR-146b, miR-1940, and miR-1298 were significantly overexpressed in colons of C. difficile-infected mice Overall design: Colon of uninfected and C.difficile-infected C57BL6/J WT mice were sampled at day 4 post-infection with Clostridium difficile VPI 10463. The infection dose was 107 cfu/mouse.
Publication Title
Modeling the role of peroxisome proliferator-activated receptor γ and microRNA-146 in mucosal immune responses to Clostridium difficile.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 32 Downloadable Samples
- Illumina 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
View Samples- Rattus norvegicus
- 6 Downloadable Samples
Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
We used adult male Sprague-Dawley rats (280-329 g body weight). Controls were nave rats. Ischemic rats were subjected to 1-hour occlusion of the right middle cerebral artery and 16h reperfusion.
Publication Title
CNS-border associated macrophages respond to acute ischemic stroke attracting granulocytes and promoting vascular leakage.
Sample Metadata Fields
Sex, Specimen part
View Samples- Escherichia coli
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
Exponentially growing cells and type II persister cells from the DS1-(hipQ)-strain
Publication Title
Novel protocol for persister cells isolation.
Sample Metadata Fields
Specimen part, Disease, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
THREE INDEPENDENT REPLICATES AND ARE THE CONTROL NON-INFECTED CELLS:
Publication Title
Modulation of NB4 promyelocytic leukemic cell machinery by Anaplasma phagocytophilum.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Membrane estrogen receptor (ER) alpha stimulates AMP kinase to suppress SREBP1 processing and lipids in liver
Publication Title
Estrogen reduces lipid content in the liver exclusively from membrane receptor signaling.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 91 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
PURPOSE
Publication Title
Gene expression profiling reveals novel biomarkers in nonsmall cell lung cancer.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
To identify potential targets of miR-34a, we performed transcriptional profiling on proneural TS543 GBM cells, focusing on mRNAs whose levels decreased in response to miR-34a transfection as compared to control oligonucleotide.
Publication Title
miR-34a repression in proneural malignant gliomas upregulates expression of its target PDGFRA and promotes tumorigenesis.
Sample Metadata Fields
Cell line, Treatment
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Systemic hypertension increases cardiac workload and subsequently induces signaling networks in heart that underlie myocyte growth (hypertrophic response) through expansion of sarcomeres with the aim to increase contractility. However, conditions of increased workload can induce both adaptive and maladaptive growth of heart muscle. Previous studies implicate two members of the AP-1 transcription factor family, junD and fra-1, in regulation of heart growth during hypertrophic response. In this study, we investigate the function of the AP-1 transcription factors, c-jun and c-fos, in heart growth. Using pressure overload-induced cardiac hypertrophy in mice and targeted deletion of Jun or Fos in cardiomyocytes, we show that c-jun is required for adaptive cardiac hyphertrophy, while c-fos is dispensable in this context. c-jun promotes expression of sarcomere proteins and suppresses expression of extracellular matrix proteins. Capacity of cardiac muscle to contract depends on organization of principal thick and thin filaments, myosin and actin, within the sarcomere. In line with decreased expression of sarcomere-associated proteins, Jun-deficient cardiomyocytes present disarrangement of filaments in sarcomeres and actin cytoskeleton disorganization. Moreover, Jun-deficient hearts subjected to pressure overload display pronounced fibrosis and increased myocyte apoptosis finally resulting in dilated cardiomyopathy. In conclusion, c-jun but not c-fos is required to induce a transcriptional program aimed at adapting heart growth upon increased workload.
Publication Title
The AP-1 transcription factor c-Jun prevents stress-imposed maladaptive remodeling of the heart.
Sample Metadata Fields
No sample metadata fields
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