Show pageBacklinksCite current pageExport to PDFBack to top This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong. =====IgLON===== IgLONs are members of the [[immunoglobulin superfamily]] of [[cell adhesion]] [[protein]]s implicated in the process of [[neuronal outgrowth]], [[cell adhesion]] and subdomain target recognition. IgLONs form homophilic and heterophilic complexes on the cell surface that repress or promote growth depending on the neuronal population, the developmental stage and surface repertoire of IgLON family members. In a study, Sanz et al. identified a metalloproteinase-dependent mechanism necessary to promote growth in embryonic [[dorsal root ganglion]] cells (DRGs). Treatment of embryonic DRG neurons with pan-metalloproteinase inhibitors, tissue inhibitor of metalloproteinase-3, or an inhibitor of ADAM Metallopeptidase Domain 10 (ADAM10) reduces outgrowth from DRG neurons indicating that metalloproteinase activity is important for outgrowth. The IgLON family members Neurotrimin (NTM) and Limbic System-Associated Membrane Protein (LSAMP) were identified as ADAM10 substrates that are shed from the cell surface of DRG neurons. Overexpression of LSAMP and NTM suppresses outgrowth from DRG neurons. Furthermore, LSAMP loss of function decreases the outgrowth sensitivity to an ADAM10 inhibitor. Together our findings support a role for ADAM-dependent shedding of cell surface LSAMP in promoting outgrowth from DRG neurons ((Sanz RL, Ferraro GB, Girouard MP, Fournier AE. Ectodomain shedding of Limbic System-Associated Membrane Protein (LSAMP) by ADAM Metallopeptidases promotes neurite outgrowth in DRG neurons. Sci Rep. 2017 Aug 11;7(1):7961. doi: 10.1038/s41598-017-08315-0. PubMed PMID: 28801670. )). iglon.txt Last modified: 2024/06/07 02:49by 127.0.0.1