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. 1999 Oct 18;147(2):375–388. doi: 10.1083/jcb.147.2.375

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© 1999 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Comparison of the effect of IG2 on different growth substrates and to the change in growth cone morphology induced by blocking the integrin receptor. Anti-NCAM was used as polyclonal control antibody (D–F). After removal of glial endfeet IG2 no longer has an effect on growth cone morphology (compare A–C with G–I), meaning that the ligand must be located on the glial endfeet. Axon growth is largely mediated via the integrin receptor. Laminin, one of the integrin ligands is located in the ECM. Therefore, blockage of the integrin receptor β-subunit results in an effect on all substrates (J–O) that is dose-dependent (compare J–L with M–O). Interestingly growth cones are less affected in the presence of glial endfeet (J and M). Bar, 0.02 mm.