title: Role of L1CAM for axon sprouting and branching.
abstract: The central nervous system (CNS) has been traditionally considered as an organ that fails to regenerate in response to injury. Indeed, the lesioned CNS faces a number of obstacles during regeneration, including an overall non-permissive environment for axonal regeneration. However, research during the last few decades has identified axon sprouting as an anatomical correlate for the regenerative capability of the CNS to establish new connections. The immunoglobulin superfamily member L1CAM has been shown to promote the capability of neurons for regenerative axon sprouting and to improve behavioral outcomes after CNS injury. Here, we discuss the cell-autonomous role of L1CAM for axon sprouting in experimental rodent injury models and highlight the molecular interactions of L1CAM with ankyrins, ezrin-radixin-moesin proteins and the Sema3A/Neuropilin ligand-receptor complex in the context of axonal branching.
authors.affiliation: Klinik für Anästhesiologie, Universitätsmedizin Mainz, 55131 Mainz, Germany. michael.schaefer@unimedizin-mainz.de
authors.forename: Michael K E
authors.initials: MK
authors.lastname: Schäfer
authors.forename: Michael
authors.initials: M
authors.lastname: Frotscher
mesh_terms: D000818:Animals; D017487:Ankyrins / Q000378:metabolism; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D003598:Cytoskeletal Proteins / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D039842:Neural Cell Adhesion Molecule L1 / Q000737:chemistry / Q000378:metabolism*
chemical_list: D017487:Ankyrins; D003598:Cytoskeletal Proteins; D039842:Neural Cell Adhesion Molecule L1