This SuperSeries is composed of the SubSeries listed below.
Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and its denucleation.
Specimen part
View SamplesGenome-wide approach to identify the cell-autonomous role of Brg1 in lens fiber cell terminal differentiation.
Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and its denucleation.
Specimen part
View SamplesDifferential expression of HSF4 in null newborn mouse and wildtype lenses was examined to identify putative downstream targets of HSF4.
Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and its denucleation.
Specimen part
View SamplesGenome-wide approach to identify the cell-autonomous role of Brg1 in lens fiber cell terminal differentiation.
Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and its denucleation.
Specimen part
View SamplesPurpose: the goal of this experiment was to identify differentially expressed genes in Six3 null, Six6 null and Six3;Six6 compound null retinas by RNAsequencing. Method: Retinas were dissected out from the following E13.5 mouse embryos: 1) WT (Six3F/F; Six6+/+); 2) Six3 KO (Six3F/F; CAGGCre-ERTM; Six6+/+); 3) Six6 KO (Six3F/F; Six6–/–); 4) DKO (Six3F/F; CAGGCre-ERTM; Six6–/–). RNA was then extracted from the retinas and profiled using RNAsequencing. Results: RNA isolated from three pairs of retinas for each genotype group (181.2-792 ng, RIN>9) was used for library preparation using KAPA RNA HyperPrep Kit with RiboErase. Sequencing was run on Illumina HiSeq 2500 in 100-bp single-end high-output mode in the Einstein Epigenomics Core Facility. About 30 million reads were generated for each sample. Each genotype group initially had three biological replicates, but one Six6 KO replicate was later removed due to over duplication. After trimming adapters with Trim Galore (v. 0.3.7), RNA-Seq reads were aligned back to mouse genome mm10 using Tophat (v. 2.0.13). The number of reads mapped back to each gene was calculated with HTseq (v.0.6.1) using Refseq gene annotation (downloaded from the UCSC genome browser in 03/17). The Cuffdiff in Cufflinks package (v. 2.2.1) was used to generate FPKM values. We identified 13498 transcripts with FPKM value >1 in at least one of samples. Deseq2 was used to determine the differentially expressed genes (DEGs) with FDR less than 0.05 as a cutoff. Overall design: Three pairs of retinas from each genotype were analyzed (n=3 biological replicates). One Six6 KO sample was later removed due to high duplication. Six3KO, Six6KO and DKO samples were compared to WT Controls (Six3F/F) using DESeq2, respectively .
Six3 and Six6 Are Jointly Required for the Maintenance of Multipotent Retinal Progenitors through Both Positive and Negative Regulation.
Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide DNA methylation as an epigenetic consequence of Epstein-Barr virus infection of immortalized keratinocytes.
Specimen part
View SamplesThe oral cavity is the persistent reservoir for EBV with lifelong infection of resident epithelial and B cells. Infection of these cell types results in distinct EBV gene expression patterns that are regulated by epigenetic modifications involving DNA methylation and chromatin structure. Such regulation of EBV gene expression relies on viral manipulation of the host epigenetic machinery that may inadvertently result in long-lasting, oncogenic host epigenetic reprogramming. To test this hypothesis in the context of EBV infection of epithelial cells, we established a transient infection model to identify the epigenetic consequences after EBV infection of immortalized normal oral keratinocytes and subsequent viral loss.
Genome-wide DNA methylation as an epigenetic consequence of Epstein-Barr virus infection of immortalized keratinocytes.
Specimen part
View SamplesThis is an integrative genome-wide approach to identify downstream networks controlled by Pax6 during mouse lens and forebrain development.
Identification of pax6-dependent gene regulatory networks in the mouse lens.
No sample metadata fields
View SamplesMyocarditis is an inflammatory disease in the heart and is mainly caused by viral infections. Viral myocarditis has been proposed to be divided into three phases; the acute viral phase, the subacute immune phase, and the chronic cardiac remodeling phase. Although individualized therapy should be applied depending on the phase, no clinical or experimental studies have found biomarkers that distinguish between the three phases of myocarditis. Theilers murine encephalomyelitis virus (TMEV) belongs to the genus Cardiovirus, and can cause myocarditis in susceptible mouse strains. Using this novel model for viral myocarditis induced with TMEV, we conducted multivariate analysis including echocardiography, serum troponin and viral RNA titration, and microarray for identifying the biomarker candidates that discriminate the three phases. Using C3H mice infected with TMEV on 4, 7, and 60 days post infection (p.i.), we conducted bioinformatics analyses, including principal component analysis (PCA) of microarray data, since our traditional cardiac and serum assays, including two-way comparison of microarray data, did not lead to the identification of a single biomarker. PCA separated heart samples clearly between the groups of 4, 7, and 60 days p.i. Representative genes contributing to the separation were as follows: 4 and 7 days p.i., innate immunity-related genes, such as Irf7, and Cxcl9; 7 and 60 days p.i., acquired immunity-related genes, such as Cd3g and H2-Aa; and cardiac remodeling-related genes, such as Mmp12 and Gpnmb. Here, sets of molecules, but not a single molecule, identified by the unsupervised PCA, were found to be useful as the phase-specific biomarkers.
Bioinformatics multivariate analysis determined a set of phase-specific biomarker candidates in a novel mouse model for viral myocarditis.
Sex, Specimen part, Time
View SamplesThis is a comparative microarray analysis of LE-AP-2a mutants vs. wild-type P0 littermate lenses.
Cell autonomous roles for AP-2alpha in lens vesicle separation and maintenance of the lens epithelial cell phenotype.
No sample metadata fields
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