The phosphorylation state of this kinase in synaptic terminals was shown to be regulated by membrane depolarization via calcineurin.

This kinase forms heterodimers with leucine zipper containing transcription factors, such as cAMP responsive element binding protein (CREB) and MYC, and thus may play a regulatory role in PKA or retinoic acid induced neuronal differentiation.

[7] MAP3K12, otherwise known as DLK, can initiate coordinated signalling cascades that culminate in the phosphorylation of C-Jun N-terminal kinases or JNK.

[9] In addition, inhibition of DLK or JNK delays radial migration and disrupts the formation of the neocortex in mice.

The absence of DLK also protects cultured mice sensory neurons from apoptosis that would normally be triggered by a lack of NGF.