Figure 6. Alex3 degradation by Wnt1 is independent of the proteasome, JNK, CAMKII and Calcineurin pathways.

(A) Proteasome inhibition with 10 µM MG-132 treatment blocks the normal turnover of Alex3 protein but not its Wnt1-induced degradation. (B) Numerous Alex3-overexpressing HEK293AD cells treated with the proteasomal inhibitor MG132 show the most severe mitochondrial aggregating phenotype. (C) Inhibition of JNK with 10 µM SP600125 (downstream effector of the Wnt/PCP pathway), CAMKII with 25 µM KN62 or Calcineurin with 10 µM Cypermetrin (downstream effectors of the Wnt/Ca²⁺ pathway) do not induce Alex3 protein degradation. Scale bar: 10 µm.