Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients.
Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction.
Specimen part, Subject
View SamplesAntibody-independent effector functions of B cells, such as antigen presentation and cytokine production, have been shown to play an important role in a variety of immune-mediated conditions such as autoimmune diseases, transplant rejection and graft-versus-host disease. Therapeutic strategies, which interfere with B cell activation could therefore be a useful addition to the current immunosuppressive armamentarium. CD40 is one of the strongest activation stimuli for B cells. The aim of this study was to characterise the gene expression changes that occurr after B cell activation via CD40.
Inhibition of protein geranylgeranylation specifically interferes with CD40-dependent B cell activation, resulting in a reduced capacity to induce T cell immunity.
Specimen part, Subject
View SamplesThis experiment contains the transcriptomic dataset that constitutes part of an integrated transcriptomic and proteomic study monitoring the response of exponential phase E. coli O157:H7 Sakai cultures upon an abrupt downshift in temperature and water activity (from 35°C aw 0.993 to 14°C aw 0.967).
Physiological Response of Escherichia coli O157:H7 Sakai to Dynamic Changes in Temperature and Water Activity as Experienced during Carcass Chilling.
Time
View SamplesTranscriptional response to virus infection in mice lacking type I and type III signaling
Transcription factor redundancy ensures induction of the antiviral state.
Specimen part, Cell line, Treatment
View SamplesMammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, the transcriptional landscape of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide expression profile of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, prioritized stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling the bioinformatics of the congenital heart disease interactome, we deconstructed disease-centric regulatory networks encoded within this cardiogenic atlas to reveal stage-specific developmental disturbances clustered on epithelial-to-mesenchymal transition (EMT), BMP regulation, NF-AT signaling, TGFb-dependent induction, and Notch signaling. Therefore, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease.
Transcriptional atlas of cardiogenesis maps congenital heart disease interactome.
Age, Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Reprogramming factor expression initiates widespread targeted chromatin remodeling.
Specimen part
View SamplesDespite rapid progress in characterizing transcription factor-driven reprogramming of somatic cells to an induced pluripotent stem (iPS) cell state, many mechanistic questions still remain. To gain insight into the earliest events in the reprogramming process, we systematically analyzed the transcriptional and epigenetic changes that occur during early factor induction after discrete numbers of divisions. We observed rapid, genome-wide changes in the euchromatic histone modification, H3K4me2, at more than a thousand loci including large subsets of pluripotency or developmentally related gene promoters and enhancers. In contrast, patterns of the repressive H3K27me3 modification remained largely unchanged except for focused depletion specifically at positions where H3K4 methylation is gained. These chromatin regulatory events precede transcriptional changes within the corresponding loci. Our data provide evidence for an early, organized, and population-wide epigenetic response to ectopic reprogramming factors that clarify the temporal order through which somatic identity is reset during reprogramming.
Reprogramming factor expression initiates widespread targeted chromatin remodeling.
Specimen part
View SamplesThe goal of the study was to compare transcriptome changes in HeLa cells after infection with recombinant Thogoto virus (wild-type, ML deletioin mutant or ML SW mutant not able to interact wiith TFIIB. While wild-type virus is able to inhibit inflammatory genes, ML deletion mutant and TFIIB-non-interacting mutant lose this effect on gene transcription. Overall design: Examination of transcriptome changes in HeLa cells under steady state or after THOV infection using Illumina HiSeq.
Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity.
Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Retinoic acid-induced pancreatic stellate cell quiescence reduces paracrine Wnt-β-catenin signaling to slow tumor progression.
No sample metadata fields
View SamplesWe evaluated the change in expression of genes after treatment of stellate cells with retinoic acid to understand how the stellate cells can de-differentiate and effect their physiological behaviour in pathological conditions. We then tested the changes in the gene expression in 2D and 3D culture conditions for pancreatic stellate cells and in a pancreatic cancer model.
Retinoic acid-induced pancreatic stellate cell quiescence reduces paracrine Wnt-β-catenin signaling to slow tumor progression.
No sample metadata fields
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