A novel mechanism for Ca²⁺/calmodulin-dependent protein kinase II targeting to L-type Ca²⁺ channels that initiates long-range signaling to the nucleus.

ABSTRACT: Neuronal excitation can induce new mRNA transcription, a phenomenon called excitation-transcription (E-T) coupling. Among several pathways implicated in E-T coupling, activation of voltage-gated L-type Ca²⁺ channels (LTCCs) in the plasma membrane can initiate a signaling pathway that ultimately increases nuclear CREB phosphorylation and, in most cases, expression of immediate early genes. Initiation of this long-range pathway has been shown to require recruitment of Ca²⁺-sensitive enzymes to a nanodomain in the immediate vicinity of the LTCC by an unknown mechanism. Here, we show that activated Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) strongly interacts with a novel binding motif in the N-terminal domain of Ca_V1 LTCC α1 subunits that

SUBMITTER: Wang X 

PROVIDER: S-EPMC5655510 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature