PubMed 25109776
Referenced in: none
Automatically associated channels: none
Title: CK2 accumulation at the axon initial segment depends on sodium channel Nav1.
Authors: Y E Hien, A Montersino, F Castets, C Leterrier, O Filhol, H Vacher, B Dargent
Journal, date & volume: FEBS Lett., 2014 Sep 17 , 588, 3403-8
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25109776
Abstract
Accumulation of voltage-gated sodium channel Nav1 at the axon initial segment (AIS), results from a direct interaction with ankyrin G. This interaction is regulated in vitro by the protein kinase CK2, which is also highly enriched at the AIS. Here, using phosphospecific antibodies and inhibition/depletion approaches, we showed that Nav1 channels are phosphorylated in vivo in their ankyrin-binding motif. Moreover, we observed that CK2 accumulation at the AIS depends on expression of Nav1 channels, with which CK2 forms tight complexes. Thus, the CK2-Nav1 interaction is likely to initiate an important regulatory mechanism to finely control Nav1 phosphorylation and, consequently, neuronal excitability.