Description
The goal of the study was to characterize the mechanism by which Raptinal induces apoptosis using a genome-wide pooled shRNA screen. Following drug treatment, the abundance of the shRNA constructs were determined and compared between DMSO and Raptinal-treated samples. Constructs depleted in Raptinal samples versus DMSO control, are expected to potentiate Raptinal-induced apoptosis by down regulating anti-apoptotic proteins. In contrast, shRNA constructs enriched upon Raptinal treatment are expected to target pro-apoptotic proteins, whose down regulation confers protection from Raptinal-induced apoptosis. Follow up experiments were performed on enriched shRNAs in order to validate potentially novel pro-apoptotic proteins.