This SuperSeries is composed of the SubSeries listed below.
Chd7 is indispensable for mammalian brain development through activation of a neuronal differentiation programme.
Specimen part, Treatment
View SamplesWe performed array-based expression profiling to determine genes regulated by Chd7 and Top2b in CGNs. Our data show Chd7 and Top2b coregulate a common set of neuronal genes.
Chd7 is indispensable for mammalian brain development through activation of a neuronal differentiation programme.
Specimen part, Treatment
View SamplesCalyx of Held giant presynaptic terminals in the medial nucleus of the trapezoid body of the auditory brainstem form axosomatic synapses that have advanced to one of the best-studied synaptic system of the mammalian brain. As the auditory system matures and adjusts to high fidelity synaptic transmission, the calyx undergoes extensive structural and functional changes: it is formed around postnatal day 3 (P3), achieves immature function until hearing onset around P10 and can be considered mature from P21 onwards. This setting provides the unique opportunity to examine the repertoire of genes driving synaptic structure and function.
Gene expression profile during functional maturation of a central mammalian synapse.
Specimen part
View SamplesBy using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell line L-428 after knock-down of DUSP5 (dual specificity phosphatase 5)
Expression of dual-specificity phosphatase 5 pseudogene 1 (DUSP5P1) in tumor cells.
Specimen part, Cell line
View SamplesBy using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell lines.
Gene expression profiles of Hodgkin's lymphoma cell lines with different sensitivity to cytotoxic drugs.
Cell line
View SamplesMechanical unloading by ventricular assist devices (VAD) leads to significant gene-expression changes often summarized as reverse remodeling. However, little is known on individual transcriptome changes during VAD-support and its relationship to non-failing hearts (NF). In addition no data are available for the transcriptome regulation during non-pulsatile VAD-support. Therefore we analysed the gene-expression patterns of 30 paired samples from VAD-supported (including 8 non-pulsatile VADs) and 8 non-failing control hearts (NF) using the first total human genome-array available.
Global gene expression analysis in nonfailing and failing myocardium pre- and postpulsatile and nonpulsatile ventricular assist device support.
Sex, Age, Specimen part, Disease
View SamplesGrowth factors (GFs) suppression by steroid hormones recurs in embryology and is co-opted in pathology. While studying mammary cell migration, which is stimulated by GFs and antagonized by glucocorticoids (GCs), we found that GCs inhibit positive feedback loops activated by GFs and stimulate the reciprocal negative loops. Although no alterations in DNA methylation accompany the transcriptional events instigated by either stimulus, forced demethylation of distal regions broadened the repertoire of inducible genes. Our data indicate that the crosstalk involve transcription factors like p53 and NF-kB, along with reduced pausing (and traveling) of RNA polymerase II (RNAPII) at the promoters (and bodies) of GF-inducible genes. In addition, while GFs hyper-acetylated chromatin at unmethylated promoters and enhancers of genes involved in motility, GCs hypo-acetylated the corresponding regions. In conclusion, stably unmethylated genomic regions that encode feedback regulatory modules and differentially recruit RNAPII and acetylases/deacetylases underlie suppression of growth factor signaling by glucocorticoids. Overall design: RNA-Seq – EGF treatemnt for 60 min of WT and DNMT1a and DNMT3b double-knockout HCT116 cells
Epigenetic mechanisms underlie the crosstalk between growth factors and a steroid hormone.
Treatment, Subject
View SamplesAnalysis of GPR120 which play roles for the fatty acid sensor in adipose tissue. Results provide insight into the transcriptional effects caused by the loss of the GPR120 proteins and provide further insight into their functions.
Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human.
Specimen part, Treatment, Subject
View Samples