Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Time Course of Individuals Vaccinated with YF-17D

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE13484: Profiling 11,639 genes in PBMCs from 2 donors: U133 A 2.0 Custom CDF Version 9 GSE13485: Profiling 20,077 genes in 25 vaccine recipients: U133 Plus 2.0, Custom CDF Version 9 Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Troy Querec

PROVIDER: E-GEOD-13486 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Systems biology approach predicts immunogenicity of the yellow fever vaccine in humans.

Querec Troy D TD Akondy Rama S RS Lee Eva K EK Cao Weiping W Nakaya Helder I HI Teuwen Dirk D Pirani Ali A Gernert Kim K Deng Jiusheng J Marzolf Bruz B Kennedy Kathleen K Wu Haiyan H Bennouna Soumaya S Oluoch Herold H Miller Joseph J Vencio Ricardo Z RZ Mulligan Mark M Aderem Alan A Ahmed Rafi R Pulendran Bali B

Nature immunology 20081123 1

A major challenge in vaccinology is to prospectively determine vaccine efficacy. Here we have used a systems biology approach to identify early gene 'signatures' that predicted immune responses in humans vaccinated with yellow fever vaccine YF-17D. Vaccination induced genes that regulate virus innate sensing and type I interferon production. Computational analyses identified a gene signature, including complement protein C1qB and eukaryotic translation initiation factor 2 alpha kinase 4-an orche ...[more]

PMID: 19029902

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Project description:Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of multiple fluid-filled cysts that destroy the kidney architecture resulting in end-stage renal failure. Mutations in the ADPKD genes PKD1 and PKD2 account for nearly all the cases of ADPKD. Increased cell proliferation is one of the key features of the disease. Several studies indicated that polycystin-1, the product of PKD1, regulates cellular proliferation through various signaling pathways, but little is known about the role played by polycystin-2, the product of PKD2. Recently, it was reported that as with polycystin-1, polycystin-2 can acts as a negative regulator of cell growth by modulating the levels of the cyclin-dependent kinase inhibitor, p21 and the activity of the cyclin-dependent kinase 2, Cdk2. In this study we utilized different kidney cell lines expressing wild-type and mutant PKD2 as well as primary tubular epithelial cells isolated from a PKD transgenic rat to further explore the contribution of the p21/Cdk2 pathway in ADPKD proliferation. Surprisingly, over-expression of wild-type PKD2 in renal cell lines failed to inactivate Cdk2 activity and consequently had no effect on cell proliferation. On the other hand, expression of mutated PKD2 augmented proliferation only in the primary tubular epithelial cells of a rat model but this was independent of STAT-1/p21 pathway. Genome-wide expression analysis in these cells revealed that expression of the cyclin-dependent kinase inhibitor, p57 is downregulated, while p21 remains unchanged. This p57 reduction is accompanied by an increase in Cdk2 levels. Our results indicate the probable involvement of p57 on epithelial cell proliferation in polycystic kidney disease. In addition, it confirms that PKD2-induced proliferation is a multifactorial process. We used microarrays to study the modulation of gene expression by mutated PKD2 in the primary tubular epithelial cells of a transgenic rat mode Keywords: transgene Gene expression in the primary tubular epithelial of a transgenic rat mode with mutated PKD2 was compared with that of SD control rats

Project description:While pathogen-induced immunity is comparatively well characterized, far less is known about plant defense responses to arthropod herbivores. To date, most molecular-genetic studies of plant-arthropod interactions have focused on insects. However, plant-feeding (phytophagous) mites are also pests of diverse plants, and mites induce different patterns of damage to plant tissues than do well-studied insects (e.g., Lepidopteran larvae or aphids). The two-spotted spider mite, Tetranychus urticae, is among the most significant mite pests in agriculture. T. urticae is an extreme generalist that has been documented on a staggering number of plant hosts (more than 1,100), and is renowned for the rapid evolution of pesticide resistance. To understand reciprocal interactions between T. urticae and a plant host at the molecular level, we examined mite herbivory using Arabidopsis thaliana. Despite differences in feeding guilds, we found that transcriptional responses of A. thaliana to mite herbivory generally resembled those observed for insect herbivores. In particular, defense to mites was mediated by jasmonic acid (JA) biosynthesis and signaling. Further, indole glucosinolates dramatically increased mite mortality and development times. Variation in both basal and activated levels of these defense pathways might also explain differences in mite damage and feeding success between A. thaliana accessions. On the herbivore side, a diverse set of genes associated with detoxification of xenobiotics was induced upon exposure to increasing levels of in planta indole glucosinolates. Our findings provide molecular insights into the nature of, and response to, herbivory for a representative of a major class of arthropod herbivores. We used microarray to assess global gene expresion in Arabidopsis thaliana upon Tetranychus urticae attack in two A. thaliana accessions: Bla-2, resistant to spider mite herbivory and Kon, susceptible to spider mite herbivory. 3 week old Arabidopsis thaliana plants were subjected to Tetranychus urticae attack through application of 10 mites for various periods of time (timecourse scenario) or hundreds of mites for 1 hour (feeding site scenario).

Dataset Information

Time Course of Individuals Vaccinated with YF-17D

Publications

Systems biology approach predicts immunogenicity of the yellow fever vaccine in humans.

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