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Over-expressed levels of MLK1 could be causing preferential activation of the JNK pathway. Rac1 or Cdc42 relieves MLK1 autoinhibiton and allows MLK1 to dimerise, autophosphorylate and activate the MKK7/JNK/c-Jun pathway, and possibly the MKK4/p38 and MKK4/JNK/c-Jun pathways. Wild-type E1A Ad 12S is known to inhibit Ras-mediated activation of Rac1 and Cdc42. The E1B 19K protein can activate the MKK7/JNK/c-Jun pathway; this could possibly be via MLK1.
