Abstract
Cdk5 has been implicated in a multitude of processes in neuronal development, cell biology and physiology. These influence many neurological disorders, but the very breadth of Cdk5 effects has made it difficult to synthesize a coherent picture of the part played by this protein in health and disease. In this review, we focus on the roles of Cdk5 in neuronal function, particularly synaptic homeostasis, plasticity, neurotransmission, subcellular organization, and trafficking. We then discuss how disruption of these Cdk5 activities may initiate or exacerbate neural disorders. A recurring theme will be the sensitivity of Cdk5 sequelae to the precise biological context under consideration.
Highlights
Cyclin-dependent kinase 5 (Cdk5) is a protein serine, threonine kinase that regulates neuronal migration, neurite extension and compartmentalization [1,2,3], both pre- and post-synaptic aspects of neurotransmission [4,5] and synaptic plasticity [6]
We summarize the roles that Cdk5 plays in synaptic homeostasis, plasticity, neurotransmission, synaptic position, and intracellular trafficking, with an eye to gaining insight into how disruption of these activities of Cdk5 contributes to neural disease
Neuronal physiology depends on a series of balancing acts: excitation vs inhibition, stability vs turnover, transmitter release vs recycling, transport towards vs away from the soma and many others
Summary
Cyclin-dependent kinase 5 (Cdk5) is a protein serine, threonine kinase that regulates neuronal migration, neurite extension and compartmentalization [1,2,3], both pre- and post-synaptic aspects of neurotransmission [4,5] and synaptic plasticity [6]. It is interesting that Cdk5 phosphorylation of PCTAIRE1 impedes dendrite development, potentially linking a mechanism that regulates synaptic physiology with one that controls neuron structure directly [28]. Cdk5-dependent phosphorylation targets numerous proteins for degradation by the (UPS) as well as regulating its activity [50,51,52].
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