Project description:We report the transcriptional changes associated with treatment of U2OS osteosarcoma cell line with DMSO, AML108, AMN107, BGW675, JAA804, LEE837 and LHD510.
Project description:CRISPR screen: U2OS or U2OS p53KO cells expressing Cas9 were transduced with a whole-genome library of CRISPR sgRNAs, then treated with either DMSO or etoposide. Differential sgRNA abundances were calculated for each condition and used to determine the effect of each single gene knockout on fitness and the drug-induced death rate. RNA-Seq: U2OS or U2OS p53KO cells were cultured with either DMSO or etoposide for 48 hours, and then U2OS cells were incubated in this conditioned media for 8 hours. RNA was collected and use to observe differential expression changes between conditions.
Project description:To better understand the mechanism by which CFZ impacts polyQ toxicity, we conducted a transcriptomic analysis in polyQ94-EGFP expressing U2OS (5μM, 8 days). Data from a transcriptomics experiment in polyQ94-U2OS cells treated with CFZ (5 μM, 8day) was compared to a DMSO-treated control.
Project description:To treat obesity and its related metabolism, small molecules can be used. To investigate the role of small molecules, butein, sulfuretin, and resveratrol were treated in differentiated adipocytes to find important regulators in adipocyte biology. Each small molecules have their own charactaristics on adipocyte biology, comparison of expression profiles among three small molecules can offer new insight in adipocyte biology.
Project description:The mitochondrial respiratory chain assembles into higher order complexes termed supercomplexes (SCs) under certain physiological or metabolic stimuli. A small molecule screen developed by the lab identified DHODH inhibitors as potent activators of SC assembly in cancer cells. To investigate the proteomic regulation of SCs under nucleotide deficiency, we treated U2OS cells for 48 hours with Brequinar (500 nM). Proteomic analysis highlighted strong signatures of respiratory chain subunit abundance and peroxisomal-derived ether phospholipid synthesis enzymes. Bypassing DHODH inhibition through uridine supplementation prevented these alterations. These findings establish a coordinated cellular response to reduced nucleotide pools that stimulates ether phospholipid synthesis and respiratory chain supra-assembly.