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. Author manuscript; available in PMC: 2018 Jun 19.
Published in final edited form as: J Biol Chem. 2001 Nov 7;277(5):3530–3536. doi: 10.1074/jbc.M107031200

FIG. 7. Treatment with oligodeoxynucleotides antisense to MEKK1, 2, or 4 blocks the ability of Q226L Gα13 to activate JNK1 activity.

FIG. 7

Cells were transiently transfected with empty vector (EV), the expression vector harboring Q226L Gα13 alone, or the empty vector and the Q226L Gα13 vector in combination with the oligodeoxynucleotides antisense to MEKK1–4. Cells were treated for 12 h prior with the antisense ODNs and transiently transfected with the empty vector (pCDNA3) or expression vector harboring Q226L Gα13 for the next 48 h in the presence of the antisense ODNs. The ODNs were replenished every 24 h for the entire 60-h period. At the end of the transient transfection, JNK1 activity, JNK expression, Gα13 immunoreactivity, and PE formation were assayed in the cells (A). The results shown are representative of at least three separate experiments. The amounts of MEKK1, MEKK2, MEKK3, and MEKK4 were determined by immunoblotting for all of the clones treated with antisense ODNs specifically targeting one of the MEKK family (B). A representative experiment is displayed. The suppression of MEKK forms in response to treatment with antisense ODNs under these conditions ranged from 70–85%.