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Juxtaparanodal clustering of Shaker-like K+ channels in myelinated axons depends on Caspr2 and TAG-1

  1. Author:
    Poliak, S.
    Salomon, D.
    Elhanany, H.
    Sabanay, H.
    Kiernan, B.
    Pevny, L.
    Stewart, C. L.
    Xu, X. R.
    Chiu, S. Y.
    Shrager, P.
    Furley, A. J. W.
    Peles, E.
  2. Author Address

    Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel Univ Sheffield, Sch Med & Biomed Sci, Ctr Dev Genet, Sheffield S10 2TN, S Yorkshire, England NCI, Canc & Dev Biol Lab, Frederick, MD 21702 USA Univ Rochester, Med Ctr, Dept Neurobiol & Anat, Rochester, NY 14642 USA Univ Wisconsin, Sch Med, Dept Physiol, Madison, WI 53706 USA Peles E Weizmann Inst Sci, Dept Mol Cell Biol, IL-76100 Rehovot, Israel
    1. Year: 2003
  1. Journal: Journal of Cell Biology
    1. 162
    2. 6
    3. Pages: 1149-1160
  2. Type of Article: Article
  1. Abstract:

    In myelinated axons, K+ channels are concealed under the myelin sheath in the juxtaparanodal region, where they are associated with Caspr2, a member of the neurexin superfamily. Deletion of Caspr2 in mice by gene targeting revealed that it is required to maintain K+ channels at this location. Furthermore, we show that the localization of Caspr2 and clustering of K channels at the juxtaparanodal region depends on the presence of TAG-1, an immunoglobulin-like cell adhesion molecule that binds Caspr2. These results demonstrate that Caspr2 and TAG-1 form a scaffold that is necessary to maintain K+ channels at the juxtaparanodal region, suggesting that axon-glia interactions mediated by these proteins allow myelinating glial cells to organize ion channels in the underlying axonal membrane.

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