Skip to main content
. Author manuscript; available in PMC: 2008 Apr 30.
Published in final edited form as: Cancer Cell. 2007 May;11(5):447–460. doi: 10.1016/j.ccr.2007.03.009

Figure 6. ERK induces JNK activation as part of cross-talk and feed-forward mechanisms.

Figure 6

A. Inhibition of the MEK/ERK pathway affects RACK1 and P-JNK levels. A375 cells were treated with 50μM PD98059 (PD) or 10μM of JNK inhibitor for the indicated times. Protein samples were analyzed by Western blots using the indicated antibodies. α-Tubulin reveals equal loading.

B. Inhibition of the MEK/ERK pathway affects c-Jun, P-JNK and cyclin D1 levels. The indicated melanoma cell lines were treated with 50μM PD98059 for 16h. Protein samples were analyzed by Western blots using the indicated antibodies. α-Tubulin reveals equal loading.

C. Inhibition of c-Jun attenuates JNK activity in SW1 mouse melanoma cells. SW1 cells were transfected to establish stable clones expressing the dominant negative form of c-Jun, TAM67. Cells were used to monitor JNK phosphorylation on aa 183/5, which reflect JNK activity.

D. c-Jun regulates cyclin D1 expression. Protein extracts from Lu1205 and SW1 cells stably transfected with FLAG-TAM67 were blotted with the indicated antibodies. α-Tubulin antibody was used to monitor equal protein loading.

E. LiCl restores c-Jun and cyclin D1 levels that are reduced by MEK/ERK inhibitors. Lu1205 cells were treated with 50μM PD98059 (PD) in the presence or absence of 10mM LiCl for 12h. Protein samples were analyzed by Western blots using the indicated antibodies. α-Tubulin reveals equal loading.

F. CREB siRNA affects both c-Jun and cyclin D1 protein levels in melanoma. Protein extracts from A375SM cells stably transfected with non-targeting vector (NT) or with a vector encoding CREB siRNA were analyzed by Western blots using the indicated antibodies. α-Tubulin reveals equal loading.