p38α, but not p38β, mediated the stimulatory effect of PRMT1 on erythroid differentiation.

<p>(A) Stable expression of shRNAs specific for either p38α or p38β depleted p38α and p38β proteins in K562 cells, respectively. Luc represents the luciferase control cell clone. Knocking down p38α (p38α KD) significantly suppressed araC-induced erythroid differentiation, whereas knockdown of p38β (p38β KD) had no apparent effect. (B) Consistently, ectopic expression of Flag-p38α enhanced erythroid differentiation, whereas Flag-p38β had no effect. (C) The ectopically expressed Flag-p38α and Flag-p38β proteins exhibited similar kinase activity upon sorbitol stimulation, indicating that they are both functionally active enzymes. (D) In p38α KD cell clones, ectopic expression of HA-PRMT1 failed to enhance araC-induced erythroid differentiation; however, HA-PRMT1 still retained its stimulatory effects in p38β KD cell clones. (E) Notably, Flag-p38α effectively stimulated araC-induced erythroid differentiation even in the PRMT1-deficient cell clones KD1 and KD2. 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 control cells.