The endoplasmic reticulum (ER) is the site of secretory lipoprotein production and de novo cholesterol synthesis, yet little is known about how these activities are coordinated with each other, or with the activity of the COPII machinery, which transports ER cargo to the Golgi. The Sar1B component of this machinery is mutated in Chylomicron Retention Disorder, establishing that this Sar1 isoform secures delivery of dietary lipids into the circulation.
The endoplasmic reticulum coat protein II transport machinery coordinates cellular lipid secretion and cholesterol biosynthesis.
No sample metadata fields
View SamplesTo explore the molecular basis for TSC22D4 function in hepatic lipid homeostasis in vivo TSC22D4 was knocked down in the mouse liver using adenovirus and performed genome wide expression analysis.
TSC22D4 is a molecular output of hepatic wasting metabolism.
Specimen part
View SamplesIdentify genes in the aorta whose expressions under genetic regulation in the Hybrid Mouse Diversity Panel (HMDP). The HDMP is comprised of classical inbred and recombinant inbred wild-type mice. The RMA values of genes were used for genome-wide association as described in Bennett et al. Genome Research 2010 (PMID 20054062). These data were used to identify candidate genes at loci associated with atherosclerosis.
High-resolution association mapping of atherosclerosis loci in mice.
Sex, Age, Specimen part
View SamplesWe used microarrays to detail the global programme of gene expression upon the over-expression of seven different differentiation-associated, E1A-regulated microRNAs.
Differentiation-associated microRNAs antagonize the Rb-E2F pathway to restrict proliferation.
Cell line
View SamplesProliferating C2C12 myoblasts were induced to differentiate into myotubes and then infected with adenovirus expressing E1A (Ad-E1A), which induces cell cycle re-entry and dedifferentiation.
Differentiation-associated microRNAs antagonize the Rb-E2F pathway to restrict proliferation.
Specimen part, Cell line, Treatment, Time
View SamplesThe therapeutic potential of pro-resolution factors in determining the outcome of inflammatory events has gained ground over the past decade. However, the attention has been focused on the non-genomic effects of these endogenous, anti-inflammatory substances. In this study, we have focused our attention on identifying specific annexin 1 (AnxA1) protein/ALX receptor mediated gene activation, in an effort to identify down-stream genomic targets of this well-known, glucocorticoid induced, pro-resolution factor.
Downstream gene activation of the receptor ALX by the agonist annexin A1.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Requirement for the histone deacetylase Hdac3 for the inflammatory gene expression program in macrophages.
Specimen part, Treatment
View SamplesPan-Hdac inhibitors (HDACi) are endowed with a potent anti-inflammatory activity, but the relative role of each of the eleven Hdac proteins sensitive to HDACi to the inflammatory gene expression program is unknown. Using an integrated genomic approach we found that Hdac3-deficient macrophages are unable to activate almost half of the inflammatory gene expression program when stimulated with lipopolysaccharide (LPS). A large part of the activation defect is due to loss of basal and LPS-inducible expression of IFNb, which in basal cells maintains Stat1 protein levels, and after stimulation acts in an autocrine/paracrine manner to promote a secondary wave of Stat1-dependent gene expression. We show that loss of Hdac3-mediated repression of nuclear receptors leads to hyperacetylation of thousands of genomic sites and associated gene derepression. The upregulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), has a causative role in the phenotype, since its chemical inhibition reverts the Ifnb activation defect. These data may have relevance for the use of selective Hdac inhibitors as anti-inflammatory agents.
Requirement for the histone deacetylase Hdac3 for the inflammatory gene expression program in macrophages.
Specimen part, Treatment
View SamplesIn this study, we analyzed the impact of a mutation in the wrn-1 gene compared to wild type worms and the dietary supplementation of vitamin C on the global mRNA expression of the whole C. elegans by the RNA-seq technology. Overall design: Whole C. elegans mRNA profiles at the L4 stage of wild type and wrn-1(gk99) mutant animals treated with or without 10 mM ascorbate were generated by deep sequencing, in triplicate, using the HiSeq 2000 machine form Illumina. Detailed statistics on the quality of the reads were calculated with FastQC (http://www.bioinformatics.babraham.ac.uk/projects/fastqc/). The 50 base pairs raw sequences were aligned on the C. elegans ce10/W220 genome with TopHat using the Ensembl annotations provided with the Illumina iGenomes. The htseq-count software (http://www-huber.embl.de/users/anders/HTSeq) was used to count the number of reads aligned to each gene. These counts were then normalized relative to the sequencing depth with DESeq.
Expression profile of Caenorhabditis elegans mutant for the Werner syndrome gene ortholog reveals the impact of vitamin C on development to increase life span.
Specimen part, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Oxidative stress activates a specific p53 transcriptional response that regulates cellular senescence and aging.
Age, Specimen part
View Samples