IL-4/GFP- enhanced transcript (4Get) reporter mice were infected with 200 PFU of Influenza A virus PR8 strain. At day 3 of infection, mediastinal lymph nodes were harvested and GFP+ cells sorted and separated by their ability to bind a CD1d-tetramer (Tet+ n=133 , Tet- n=109 ). Single-cell RNA-Seq was used to identify subpopulations of IL-4 producing cells. Single-cell transcriptomes were clustered using Seurat and differentially expressed genes within each cluster were used to resolve IL-4+ subpopulations and aid in defining their role in initiating B cell immunity during influenza infection. Overall design: Examine cells involved in accute viral response in the lymph node after influenza infection
Initiation of Antiviral B Cell Immunity Relies on Innate Signals from Spatially Positioned NKT Cells.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Critical role for TRIM28 and HP1β/γ in the epigenetic control of T cell metabolic reprograming and effector differentiation.
Specimen part
View SamplesCritical role for TRIM28 and HP1b/g in the epigenetic control of T cell metabolic reprogramming and effector differentiation
Critical role for TRIM28 and HP1β/γ in the epigenetic control of T cell metabolic reprograming and effector differentiation.
Specimen part
View SamplesCritical role for TRIM28 and HP1b/g in the epigenetic control of T cell metabolic reprogramming and effector differentiation
Critical role for TRIM28 and HP1β/γ in the epigenetic control of T cell metabolic reprograming and effector differentiation.
Specimen part
View SamplesDiploid and tetraploid budding yeast cell cultures were grown in YPD, at 30C, to O.D. approx. 0.5.
Genome-wide genetic analysis of polyploidy in yeast.
Sex
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide methylation analysis in vestibular schwannomas shows putative mechanisms of gene expression modulation and global hypomethylation at the HOX gene cluster.
Specimen part
View SamplesBackground: Schwannomas and grade I meningiomas are non-metastatic neoplasms that shares the common mutation of gene NF2. They usually appear in Neurofibromatosis type 2 patients. Currently, there is no drug treatment available for both tumors, so the use of wide expression technologies is crucial to find those therapeutic targets.
Global expression profile in low grade meningiomas and schwannomas shows upregulation of PDGFD, CDH1 and SLIT2 compared to their healthy tissue.
Specimen part
View SamplesVestibular schwannomas are intracranial tumors that affects unilateral and sporadically or bilateral when is associated to Neurofibromatosis type 2 syndrome. The hallmark of the disease is the biallelic inactivation by NF2 gene mutation or LOH of chromosome 22q, where this gene harbors. In this work, we used Infinium HumanMethylation 450K BeadChip microarrays in a series of 36 vestibular schwannomas, 4 non-vestibular schwannomas and 5 healthy nerves. Our results shows a trend to hypomethylation in schwannomas. Furthermore, HOX genes, located at 4 clusters in the genome, displayed hypomethylation in numerous CpG sites in vestibular but not in non-vestibular schwannomas. Additionally, several microRNA and protein-coding genes were found hypomethylated at promoter regions and confirmed by expression analysis; including miRNA-199a1, miRNA-21, MET and PMEPA1. We also detected methylation patterns that might be involved in alternative transcripts of several genes such as NRXN1 or MBP; that would increase the complexity of methylation-expression. Overall, our results shows specific epigenetic signatures in several coding genes and microRNA that could be used in the finding of potential therapeutic targets.
Genome-wide methylation analysis in vestibular schwannomas shows putative mechanisms of gene expression modulation and global hypomethylation at the HOX gene cluster.
Specimen part
View SamplesVestibular Schwannomas are benign neoplasms that arise from the vestibular nerve. The hallmark of these tumors is the biallelic inactivation of NF2. Transcriptomic alterations, such as the Nrg1/ErbB2 pathway, have been described in Schwannomas. Here, we have performed a whole transcriptomic analysis in 31 vestibular Schwannomas and 9 control nerves in the Affymetrix Gene 1.0ST platform, validated by quantitative Real-Time PCR using TaqMan Low Density Arrays. We performed a mutational analysis of NF2 by PCR/dHPLC and MLPA as well as a microsatellite marker analysis of the loss of heterozygosity of chromosome 22q. The microarray analysis showed that 1516 genes were deregulated, and 48 of the genes were validated by qRT-PCR. At least two genetic hits (allelic loss and/or gene mutation) in NF2 were found in 16 tumors, seven cases showed one hit and eight tumors showed no NF2 alteration. As conclusion, MET and associated genes such as ITGA4/B6, PLEXNB3/SEMA5 and CAV1 showed a clear deregulation in vestibular Schwannomas. In addition, androgen receptor (AR) downregulation may denote a hormonal effect or cause in this tumor. Furthermore, the osteopontin gene (SPP1), which is involved in Merlin protein degradation, was upregulated, which suggests that this mechanism may also exert a pivotal role in Schwannoma Merlin depletion. Finally, no major differences were found between tumors of different sizes, histological types or NF2 status, which suggests that at the mRNA level all Schwannomas, regardless of molecular and clinical characteristics, may share common features that can be used in the fight against them.
Microarray analysis of gene expression in vestibular schwannomas reveals SPP1/MET signaling pathway and androgen receptor deregulation.
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View Samplesdrl expression initiates during gastrulation and condenses as a band of cells at the prospective lateral embryo margin. In late epiboly, drl:EGFP is detectable as a band of scattered EGFP-fluorescent cells; after gastrulation, drl:EGFP-positive cells coalesce at the embryo margin that then in somitogenesis break down into the anterior and posterior lateral plate with subsequent cell migrations that form the posterior vascular/hematopoietic stripes and the anterior cardiovascular and myeloid precursors.
Chamber identity programs drive early functional partitioning of the heart.
Age, Specimen part
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