Fig. 1: Deficiency in PRMT5 suppresses AKT activation.
From: PRMT5-mediated arginine methylation activates AKT kinase to govern tumorigenesis
a, b Immunoblot (IB) analysis of whole cell lysates (WCLs) derived from MCF7 cells infected with lentiCRISPR virus (a) or shRNAs virus targeting PRMT5 (b). The cells were selected with 2 μg/ml puromycin for 4 days to eliminate the non-infected cells. c IB analysis of WCLs derived from MCF7 cells treated with GSK591 for 24 h. d AKT in vitro kinase assays were performed using endogenous AKT1 (IgG as a negative control) immunopurified (IP) from control cells or sgPRMT5 cells as the kinase source and recombinant GST-GSK-3β purified from bacteria as the substrate. e IB analysis of WCLs derived from control cells or PRMT5-depleted MCF7 cells. Cells were serum-starved for 16 h and then treated with 100 nM insulin for 0, 30, and 60 min before collecting. Similar results were obtained in n ≥ 2 independent experiments in a–e. Uncropped immunoblots are provided in Source Data file.
