PT  - JOURNAL ARTICLE
AU  - Pierre-Marie Martin
AU  - Michèle Carnaud
AU  - Gontzal Garcia del Caño
AU  - Marie Irondelle
AU  - Theano Irinopoulou
AU  - Jean-Antoine Girault
AU  - Bénédicte Dargent
AU  - Laurence Goutebroze
TI  - Schwannomin-Interacting Protein-1 Isoform IQCJ-SCHIP-1 Is a Late Component of Nodes of Ranvier and Axon Initial Segments
AID  - 10.1523/JNEUROSCI.1044-08.2008
DP  - 2008 Jun 11
TA  - The Journal of Neuroscience
PG  - 6111--6117
VI  - 28
IP  - 24
4099  - http://www.jneurosci.org/content/28/24/6111.short
4100  - http://www.jneurosci.org/content/28/24/6111.full
SO  - J. Neurosci.2008 Jun 11; 28
AB  - Axon initial segments (AISs) and nodes of Ranvier (NRs) are essential regions for saltatory conduction of the action potential along the axon. These two domains are enriched in similar multimolecular complexes, which include voltage-gated sodium channels (Nav), NF186 (neurofascin 186), NrCAM (neuron glia-related cell adhesion molecule), and cytoskeleton linkers ankyrin G (AnkG) and βIV-spectrin. Identification of novel members of these complexes is critical to better understand their formation, function, and maintenance. Here we report that IQCJ-SCHIP-1, a recently identified isoform of schwannomin-interacting protein-1 (SCHIP-1), is a novel component of both AISs and NRs in the central and peripheral nervous systems. We show that IQCJ-SCHIP-1 binds calmodulin in the absence of Ca2+ and is highly enriched at AISs and NRs. IQCJ-SCHIP-1 accumulation at AISs and NRs is a late event, suggesting that IQCJ-SCHIP-1 is likely to play a role in mature AISs and NRs rather than during their formation. IQCJ-SCHIP-1 was not detected at AISs in the absence of AnkG and interacted in vitro with this protein. IQCJ-SCHIP-1 was also absent from central NRs and AISs of quivering mice, which have a mutation of βIV-spectrin. We suggest that IQCJ-SCHIP-1 might participate, along with AnkG and βIV-spectrin, in the stabilization or function of the multimolecular complexes of AISs and NRs, possibly by participating in Ca2+-mediated responses.