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. Author manuscript; available in PMC: 2009 Sep 11.
Published in final edited form as: Exp Cell Res. 2004 Dec 10;301(2):147–157. doi: 10.1016/j.yexcr.2004.07.008

Fig. 4.

Fig. 4

Conventional PKC isoforms meditate retinoid effects on EGF signaling. (A) EGF activation of EGFR autophosphorylation and of Erk 1/2 was analyzed as described above. Serum-deprived T-47D cells were pretreated with 10−7 M RA for 36 h and then stimulated with EGF for 10 min. Where indicated the inhibitor of the conventional PKCs, Gö6976 (500 nM), was added 30 min before stimulation with EGF for 10 min. In each assay, Gö6976 restored EGF signaling in RA-treated cells, implicating cPKC isoforms as mediators of the RA effect. (B) EGF activation of Erk 1/2 was compared in parental T-47D cells and in T-47D cells constitutively expressing PKCα (T47D-PKCα). EGF treatment stimulated Erk phosphor-ylation in both cell lines, but in the PKCα-expressing cells p-Erk levels returned to baseline by 30 min, whereas activation in the parental cells was sustained for at least 30 min.