Fig. 6.
Fig. 6. Role of PKCζ on DNR-induced MAPK activation. / (A) U937 cells were either untreated or preincubated in the absence or in the presence of both 10 μg/mL D609 for 30 minutes and 25 nmol/L wortmannin for 1 hour, 250 μM 8-bromo-cAMP for 30 minutes followed by 1 μM DNR for 4 minutes, and PKCζ kinase activity was measured as described in “ Materials and methods.” Results are mean ± SEM of 3 independent determinations. *P < .01 compared with cells treated with DNR alone. (B) C10 and Z4 cells were incubated with 1 μM DNR, and PKCζ kinase activity was measured as described in “ Materials and methods.” Results are mean ± SEM of 3 independent determinations. *P < .01. (C) Control cells (C10) and kinase-defective PKCζ cells (Z4) were incubated with 1 μM DNR, and ERK activation was evaluated by anti-P–MAPK as described in “Materials and methods.” Results are representative of 3 independent experiments.

Role of PKCζ on DNR-induced MAPK activation.

(A) U937 cells were either untreated or preincubated in the absence or in the presence of both 10 μg/mL D609 for 30 minutes and 25 nmol/L wortmannin for 1 hour, 250 μM 8-bromo-cAMP for 30 minutes followed by 1 μM DNR for 4 minutes, and PKCζ kinase activity was measured as described in “ Materials and methods.” Results are mean ± SEM of 3 independent determinations. *P < .01 compared with cells treated with DNR alone. (B) C10 and Z4 cells were incubated with 1 μM DNR, and PKCζ kinase activity was measured as described in “ Materials and methods.” Results are mean ± SEM of 3 independent determinations. *P < .01. (C) Control cells (C10) and kinase-defective PKCζ cells (Z4) were incubated with 1 μM DNR, and ERK activation was evaluated by anti-P–MAPK as described in “Materials and methods.” Results are representative of 3 independent experiments.

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