Project description:Aberrant activity of type II topoisomerases (TOP2) often causes blocked double-strand breaks (DSBs), whose inefficient repair can seriously compromise genomic stability. One of the two TOP2 paralogs encoded in vertebrates is TOP2B, which has been linked to essential processes such as transcription or genome organization. Few TOP2B genome-wide maps have been profiled, and a comprehensive study of the mechanisms involved in TOP2B-DNA binding is still lacking. Here, we conduct an in silico approach for the prediction of TOP2B binding sites using publicly available sequencing data. We achieve highly accurate predictions and find that open chromatin and architectural factors are the most informative features. We also validate our predictions on experimental data and generate predicted TOP2B tracks that mirror experimental ones with high precision.
Project description:Site-specific glycosylation analysis by nLC-MS/MS of recombinant human Fcγ receptors IIA (H&R167 isoforms), IIB and murine Fcγ receptor IIB.
Project description:The heat shock transcription factor, HSF1, facilitates the catalytic engagement of topoisomerase IIb (TOP2B) within the neuronal genome
Project description:RNA-Seq of human endothelial cells treated with ACF revealed massive changes on gene expression. These were non-randomly and strongly conserved to murine lung endothelial cells potentially due to DNA topoisomerase inhibition rather than HIF inhibition. Surprisingly, in contrast to protein-coding genes, RNA-Seq yielded that an exceeding number of lncRNAs is upregulated, e.g. FENDRR, H19, HIF1α-AS1 and FLJ31356, whereas BOLA3-AS1 and MEG3 were strongly downregulated. ATAC-Seq demonstrated that ACF leads to strong changes on chromatin accessibility on lncRNA promoters.
Project description:RNA-Seq of human endothelial cells treated with ACF revealed massive changes on gene expression. These were non-randomly and strongly conserved to murine lung endothelial cells potentially due to DNA topoisomerase inhibition rather than HIF inhibition. Surprisingly, in contrast to protein-coding genes, RNA-Seq yielded that an exceeding number of lncRNAs is upregulated, e.g. FENDRR, H19, HIF1α-AS1 and FLJ31356, whereas BOLA3-AS1 and MEG3 were strongly downregulated. ATAC-Seq demonstrated that ACF leads to strong changes on chromatin accessibility on lncRNA promoters.