Gene expression profiles were examined in whole lung tissue collected from male and female Long-Evans rats at different time points after inoculation with Seoul virus (i.e., the species-specific hantavirus that infects Norway rats)
Sex differences in the recognition of and innate antiviral responses to Seoul virus in Norway rats.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The response and recovery of the Arabidopsis thaliana transcriptome to phosphate starvation.
Age, Specimen part, Treatment
View SamplesBackground: Over application of phosphate fertilizers in modern agriculture contaminates waterways and disrupts natural ecosystems. Nevertheless, this is a common practice among farmers, especially in developing countries as abundant fertilizers are believed to boost crop yields. The study of plant phosphate metabolism and its underlying genetic pathways is key to discovering methods of efficient fertilizer usage. The work presented here describes the first genome-wide resource on the molecular dynamics underpinning the response and recovery in roots and shoots of Arabidopsis thaliana to phosphate-starvation. Results: Genome-wide profiling revealed minimal overlap between root and shoot transcriptomes suggesting two independent phosphate-starvation regulons. Novel gene expression patterns were detected for over 1000 candidates and were classified as either initial, persistent, or latent responders. Comparative analysis to AtGenExpress identified novel cohorts of genes co-regulated across multiple stimuli. The hormone ABA displayed a dominant role in regulating many phosphate-responsive candidates. Analysis of co-regulation enabled the determination of primary versus redundant members of closely related gene families with respect to phosphate-starvation. Thus, among others, we show that PHO1 acts in shoot, whereas PHO1;H1 is likely the primary regulator in root. Conclusion: Our results uncover a much larger, staged responses to phosphate-starvation than previously described. To our knowledge, this work describes the highest resolution of genome-wide data on plant nutrient stress to date.
The response and recovery of the Arabidopsis thaliana transcriptome to phosphate starvation.
Age, Specimen part, Treatment
View SamplesThe objective of this study was to identify transcriptional changes differentially regulated by GDF11 stimulation compared to TGFB1
Tumor-Suppressor Inactivation of GDF11 Occurs by Precursor Sequestration in Triple-Negative Breast Cancer.
Specimen part
View SamplesTissue samples have been isolated during corornary artery by-pass grafting (CABG)surgery from the atheroscelrotic arterial wall (AAW, aortic root puncture for proxmal ligation of by-pass vessel), non-atherosclertoci arterial wall (NAAW, distal part of mammary artery used a graft for LAD), liver, skeletal muscle (Recturs m), pericardial mediastinal visceral fat) in CAD patients. Carotid lesions samples from 25 validation patients.
Multi-organ expression profiling uncovers a gene module in coronary artery disease involving transendothelial migration of leukocytes and LIM domain binding 2: the Stockholm Atherosclerosis Gene Expression (STAGE) study.
Specimen part
View SamplesCD133 (Prominin1) is pentaspan transmembrane glycoprotein expressed in several stem cell populations and cancers. Reactivity with an antibody (AC133) to a glycoslyated form of CD133 has been widely used for the enrichment of cells with tumor initiating activity in xenograph transplantation assays. We have found by fluorescence-activated cell sorting that increased AC133 reactivity in human embryonic stem cells, colon cancer and melanoma cells is correlated with increased DNA content and reciprocally, that the least reactive cells are in the G1/G0 portion of the cell cycle. Continued cultivation of cells sorted on the basis of high and low AC133 reactivity results in a normalization of the cell reactivity profiles indicating that cells with low AC133 reactivity can generate highly reactive cells as they resume proliferation. The association of AC133 with actively cycling cells may contribute to the basis for enrichment for tumor initiating activity.
Cell cycle-dependent variation of a CD133 epitope in human embryonic stem cell, colon cancer, and melanoma cell lines.
No sample metadata fields
View SamplesCombining an in vitro hNCC differentiation protocol with epigenomic profiling, we provide the first whole-genome characterization of cis-regulatory elements in this highly relevant cell type. With this data at hand, we have characterized the chromatin state and dynamics of all human gene promoters during the course of NCC in vitro differentiation. Most importantly, we have identified a large cohort of active and NCC-specific enhancers, which we showed to be functionally relevant in vivo, in the context of embryonic development. Finally, through sequence analysis of the identified NCC enhancers, we uncovered the orphan nuclear receptors NR2F1 and NR2F2 as novel hNCC transcriptional regulators both in vitro and in vivo. Overall design: RNA-seq experiments in human neural crest cells (hNCC)
Epigenomic annotation of enhancers predicts transcriptional regulators of human neural crest.
No sample metadata fields
View SamplesThe lipocalin Apolipoprotein D (ApoD), known to protect the nervous system against oxidative stress (OS) in model organisms, is up-regulated early in the mouse brain in response to the ROS generator paraquat (PQ). However, the processes triggered by this up-regulation have not been explored.
Apolipoprotein D alters the early transcriptional response to oxidative stress in the adult cerebellum.
Sex, Specimen part
View SamplesA detailed knowledge of the mechanisms underlying brain aging is fundamental to understand its functional decline and the baseline upon which brain pathologies superimpose. Endogenous protective mechanisms must contribute to the adaptability and plasticity still present in the healthy aged brain. Apolipoprotein D (ApoD) is one of the few genes with a consistent and evolutionarily conserved up-regulation in the aged brain. ApoD protecting roles upon stress or injury are well known, but a study of the effects of ApoD expression in the normal aging process is still missing. Using an ApoD-knockout mouse we analyze the effects of ApoD on factors contributing to the functional maintenance of the aged brain. We focused our cellular and molecular analyses in cortex and hippocampus at an age representing the onset of senescence where mortality risks are below 25%, avoiding bias towards long-lived animals. Lack of ApoD causes a prematurely aged brain without altering lifespan. Age-dependent hyperkinesia and memory deficits are accompanied by differential molecular effects in cortex and hippocampus. Transcriptome analyses reveal distinct effects of ApoD loss on the molecular age-dependent patterns of cortex and hippocampus, with different cell-type contributions to age-regulated gene expression. Markers of glial reactivity, proteostasis, and oxidative and inflammatory damage reveal early signs of aging and enhanced brain deterioration in the ApoD-knockout brain. The lack of ApoD results in an age-enhanced significant reduction in neuronal calcium-dependent functionality markers and signs of early reduction of neuronal numbers in the cortex, thus impinging upon parameters clearly differentiating neurodegenerative conditions from healthy brain aging. Our data support the hypothesis that the physiological increased brain expression of ApoD represents a homeostatic anti-aging mechanism.
Aging without Apolipoprotein D: Molecular and cellular modifications in the hippocampus and cortex.
Sex, Age, Specimen part
View SamplesSpecific deletion of suppressor of cytokine signaling 3 (Socs3) in keratinocytes can cause severe skin inflammation with infiltration of immune cells, however the molecular mechanisms and key regulatory pathways involved remains poorly understood. To investigate the role of Socs3 in keratinocytes, we generated and analyzed global RNA-Seq profiles in Socs3 conditional knockout (cKO) mice at two different stages (2- and 10- weeks). Over 400 shared genes were found to be significantly regulated at both time points. Two week samples were marked by initial skin barrier dysfunction established by the downregulation of keratin associated genes and upregulation of genes regulating lipid metabolism. Subsequent increase in expression level of multiple chemokines and cytokines at 10 week were observed representing response to skin inflammation caused by the disruption of skin barrier function. A group of activator protein-1 related genes were to found to be highly elevated in Socs3 cKO mice at both time points. This observation was duly validated using qRT-PCR in Socs3 depleted human keratinocyte–derived HaCaT cells. Overall this study reveals an important regulatory dynamics of Socs3 in skin barrier dysfunction. Overall design: Socs3 cKO mice mRNA profiles of 2 and 10 week wild type (WT) C57BL/6 mice were generated by sequencing using HiSeq 1000 system (Illumina) machine which could read a 50 bp sequence.
Insights into gene expression profiles induced by Socs3 depletion in keratinocytes.
Age, Specimen part, Cell line, Subject
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