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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
The receptor tyrosine kinase Ror2 has recently been shown to act as an alternative receptor or coreceptor for Wnt5a and to mediate Wnt5a-induced migration of cultured cells.However, little is known about the molecular mechanism underlying this migratory process.Here we show by wound-healing assays that Ror2 plays critical roles in Wnt5a-induced cell migration by regulating formation of lamellipodia and reorientation of microtubule-organizing center (MTOC).Wnt5a stimulation induces activation of the c-Jun N-terminal kinaseJNK at the wound edge in a Ror2-dependent manner, and inhibiting JNK activity abrogates Wnt5a-induced lamellipodia formation and MTOC reorientation.Additionally, the association of Ror2 with the actin-binding protein filamin A is required for Wnt5a-inducedJNK activation and polarized cell migration.We further show that Wnt5a-inducedJNK activation and MTOC reorientation can be suppressed by inhibiting PKCzeta.Taken together, our findings indicate that Wnt5a/Ror2activatesJNK, through a process involving filamin A and PKCzeta, to regulate polarized cell migration.[1]
