Protein Arginine Methyltransferase 1 Interacts with and Activates p38α to Facilitate Erythroid Differentiation
Figure 2
Knockdown of endogenous PRMT1 proteins suppressed erythroid differentiation.
(A, upper) Endogenous PRMT1 proteins were greatly reduced in KD-1 and KD-2 cell clones that stably expressed PRMT1 shRNAs. (A, lower, B) Erythroid differentiation was significantly suppressed as detected by benzidine staining or surface expression of glycophorin A at 96 hr after induction. Luc indicates the luciferase shRNA control cells. (C) Gene expression was examined 96 hr after araC treatment by quantitative real-time PCR. Data were calculated as fold changes using vector control cells without treatment as a reference. (D) Re-introduction of HA-PRMT1 into KD-1 and KD-2 cells was performed by transient transfection and the effect on araC-induced differentiation was analyzed after 96 hr. All results shown are representative of three separate experiments. Differentiation results are presented as means ± S.E. of three repeats; *, p<0.05; **, p<0.01; ***, p<0.005 compared with vector control cells.