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. 1999 Oct;10(10):3137–3150. doi: 10.1091/mbc.10.10.3137

Figure 4.

Figure 4

Rac1 and Cdc42 are weak activators of JNK in QMb. (A) QMb were cotransfected with a HA-tagged JNK expression vector along with vectors expressing activated and dominant-negative Rho family members, MEKK1, MEKK2, and v-Src as indicated. QMb cotransfected with HA-JNK and empty vector with or without treatment with sorbitol were used as controls. The activity of immunoprecipitated HA-JNK was assayed with GST-c-Jun protein as substrate. The numbers represent fold stimulation above the activity of HA-JNK (referred to as 1) normalized for HA-JNK content. (B and C) Endogenous JNK activity was measured with glutathione beads coated with GST-c-Jun fusion protein as bait in QMb infected with RCASBP (RCAS) or RCASBP-Rac1V12 (Rac1V12) at 37°C (B) and QMb-LA29 expressing the neomycin-resistance gene (neo) at the indicated temperatures or Rac1V12 at 41°C (C). RCAS-infected QMb and QMb-LA29 were treated with UV as controls for JNK activation. Fold stimulation above basal JNK activity in RCAS-infected QMb (B) and QMb-LA29 at 41°C (C), referred to as 1, is indicated.