Project description:We profiled global gene expression in primary human umbilical vein endothelial cells to determine the gene expression changes associated with knocking down PKM2 and p53. We identified a p53 dependent transcriptional response that remodels metabolism in cells lacking p53, thus limiting cell growth. Human Umbilical Vein Endothelial Cells were transfected with siRNA duplexes targeting PKM2 and / or p53, RNA was extracted and subjected to RNA sequencing
Project description:Oxidoreductase enzymes are critical to redox regulation of intracellular proteins within human cells. We used microarrays to identify which oxidreducatse genes are expressed in unstimulated human umbilical vein endothelial cells. Human umbilical vein endothelial cells were grown under optimal conditions and then RNA extracted and hybridized on Affymetrix microarrays.
Project description:We quantified differential microRNA (miRNA) expression in Human umbilical vein endothelial cells (HUVECs)response to Angiogenin (ANG) treatment.These data were used to determine which miRNAs are altered on ANG in Human umbilical vein endothelial cells.
Project description:Oxidoreductase enzymes are critical to redox regulation of intracellular proteins within human cells. We used microarrays to identify which oxidreducatse genes are expressed in unstimulated human umbilical vein endothelial cells.
Project description:Examine the toxic effect and molecular mechanisms of PM2.5 in primary human umbilical vein endothelial cells (HUVECs) . We used microarrays to detail the global programme of gene expression in HUVECs exposed to PM2.5 and identified distinct classes of up-regulated genes.
Project description:Control ChIP-seq on human endothelial cell of umbilical vein For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:We profiled global gene expression in primary human umbilical vein endothelial cells to determine the gene expression changes associated with knocking down PKM2 and p53. We identified a p53 dependent transcriptional response that remodels metabolism in cells lacking p53, thus limiting cell growth.