This SuperSeries is composed of the SubSeries listed below.
Three human cell types respond to multi-walled carbon nanotubes and titanium dioxide nanobelts with cell-specific transcriptomic and proteomic expression patterns.
Specimen part, Cell line, Treatment, Time
View SamplesTo identify key biological pathways that define toxicity or biocompatibility after nanoparticle exposure, three human cell types were exposed in vitro to two high aspect ratio nanoparticles for 1 hr or 24 hr and collected for global transcriptomics.
Three human cell types respond to multi-walled carbon nanotubes and titanium dioxide nanobelts with cell-specific transcriptomic and proteomic expression patterns.
Specimen part, Cell line, Treatment, Time
View SamplesTo identify key biological pathways that define toxicity or biocompatibility after nanoparticle exposure, three human cell types were exposed in vitro to two high aspect ratio nanoparticles for 1 hr or 24 hr and collected for global transcriptomics.
Three human cell types respond to multi-walled carbon nanotubes and titanium dioxide nanobelts with cell-specific transcriptomic and proteomic expression patterns.
Specimen part, Cell line, Treatment, Time
View SamplesTo identify key biological pathways that define toxicity or biocompatibility after nanoparticle exposure, three human cell types were exposed in vitro to two high aspect ratio nanoparticles for 1 hr or 24 hr and collected for global transcriptomics.
Three human cell types respond to multi-walled carbon nanotubes and titanium dioxide nanobelts with cell-specific transcriptomic and proteomic expression patterns.
Specimen part, Cell line, Treatment, Time
View SamplesIt is unclear how nanosecond electrical pulses affect gene expression.
Evaluation of the Genetic Response of U937 and Jurkat Cells to 10-Nanosecond Electrical Pulses (nsEP).
Specimen part, Cell line
View SamplesIt is unclear how nanosecond electrical pulses affect gene expression.
Evaluation of the Genetic Response of U937 and Jurkat Cells to 10-Nanosecond Electrical Pulses (nsEP).
Specimen part, Cell line
View SamplesLymph node metastasis is a poor prognosis indicator in esophageal cancer. Although tumor spreading currently forms the main basis for therapy selection, the molecular mechanisms underlying the metastatic pathway remain insufficiently understood. Several studies aimed to investigate these mechanisms but focused mainly on regulatory patterns in the tumors themselves and/or the invaded lymph nodes. To date no study has yet investigated the potential changes on transcription level, which take place within the yet non-invaded niche. Here we provide a comprehensive description of these regulations in patients. In this study the transcriptomic profiles of regional lymph nodes were determined for two patient groups: patients classified as pN1 (metastasis) or pN0 (no metastasis) respectively. All investigated lymph nodes, also those from pN1 patients, were still free of metastasis. The gene expression data was obtained via microarray analysis. Top candidates were validated via PCR and immunohistochemistry. The results show that regional lymph nodes of pN1 patients differ decisively from those of pN0 patients even before metastasis has taken place. In the pN0 group distinct immune response patterns were observed. In contrast, lymph nodes of the pN1 group exhibited a clear profile of reduced immune response and reduced proliferation, but increased apoptosis, enhanced hypoplasia and morphological conversion processes. DKK1 was the most significant gene associated with the molecular mechanisms taking place in lymph nodes of patients suffering from metastasis (pN1). We assume that the two molecular profiles observed constitute two different stages of a progressive disease. Finally we suggest that DKK1 might play an important role within the mechanisms leading to lymph node metastasis.
Molecular changes in pre-metastatic lymph nodes of esophageal cancer patients.
Specimen part, Subject
View SamplesPrecise nucleosome-positioning patterns at promoters are thought to be crucial for faithful transcriptional regulation. However, the mechanisms by which these patterns are established and dynamically maintained and subsequently contribute to transcriptional control are poorly understood. The Swi/Snf (Baf) chromatin remodeling complex is a master developmental regulator and tumor suppressor that is capable of mobilizing nucleosomes in biochemical assays. Yet, its role in establishing the nucleosome landscape in vivo is unclear. Here we have inactivated Snf5 and Brg1, core subunits of the mammalian Swi/Snf complex, to evaluate their effects on chromatin structure and transcription levels genome-wide. We find that inactivation of either subunit leads to disruptions of specific nucleosome patterning combined with a loss of overall nucleosome occupancy at a large number of promoters, regardless of their association with CpG islands. These rearrangements are accompanied by gene expression changes that promote cell proliferation. Collectively, these findings define a direct relationship between chromatin-remodeling complexes, chromatin structure, and transcriptional regulation.
Swi/Snf chromatin remodeling/tumor suppressor complex establishes nucleosome occupancy at target promoters.
Specimen part
View SamplesWe generated iPSc from skin fibroblasts of two MPSIIIB patients (P1 and P2). MPSIIIB-associated cell defects were prominent in undifferentiated iPSc, in neural stem cells and in their neuronal progeny.
Modeling neuronal defects associated with a lysosomal disorder using patient-derived induced pluripotent stem cells.
Specimen part, Disease, Disease stage
View SamplesWe report high-throughput profiling of gene expression from whole zebrafish ventricles. We profile mRNA in uninjured ventricles and those undergoing regeneration 14 days after genetic ablation. This study provides a framework for understanding transcriptional changes during adult models of regeneration. Overall design: Examination of gene expression in cardiomyocytes under different states of proliferation.
Resolving Heart Regeneration by Replacement Histone Profiling.
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