Dkk2, a member of the Dikkopf family of Wnt antagonists, acts as a positive regulator of Wnt signaling during neural crest formation.

The Wnt antagonist DKK3 is a key regulator of excitatory and inhibitory synapses, and its downregulation in the hippocampus restores synaptic connectivity and memory in an Alzheimer's disease mouse model.

The regulation of the core transcription factor Oct4 by the Aurkb-PP1 axis links the cell cycle to pluripotency programs in embryonic stem cells.

DLK signaling network reveals the conserved function in neuritogenesis and synapse formation, and highlights the regulation of c-Jun translation and microtubule homeostasis in hippocampal selective neuron vulnerability.

The development and functionalities of invariant natural-killer T cells are dependent upon their cell-intrinsic ACC1-mediated de novo fatty acid synthesis, which greatly affect outcomes of allergic asthma.

The mechanism of Dbf4-dependent kinase (DDK) recruitment to replication origins and its regulation by the checkpoint have been identified.

Axonal damage sensing kinase DLK is a direct target and mediator of the cAMP effector kinase PKA in a unified mechanism for stimulating axonal regeneration.

Establishment of replication-timing involves Fkh1-dependent recruitment and execution of DDK function in G1 phase resulting in dynamic relocalization of origins within the nucleus in anticipation of CDK-dependent origin activation.

Synaptic defects previously attributed to loss of kinesin function are found to be mediated by the Wnd/DLK axonal injury signaling pathway, which restrains the total levels of presynaptic proteins in response to their accumulation.

In C. elegans and mouse neurons, the balance between poly(ADP-ribose) glycohydrolases and poly(ADP-ribose) polymerases regulates axon regeneration downstream of DLK-1/MAPKKK signaling.