{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T16:57:07Z","timestamp":1792688227435,"version":"4.5.0"},"reference-count":56,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,12,21]],"date-time":"2013-12-21T00:00:00Z","timestamp":1387584000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Glia"],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:p>Signaling through fibroblast growth factor receptors (FGFRs) is essential for many cellular processes including proliferation and migration, as well as differentiation events such as myelination. Anosmin\u20101 is an extracellular matrix (ECM) glycoprotein that interacts with the fibroblast growth factor receptor 1 (FGFR1) to exert its biological actions through this receptor, although the intracellular pathways underlying anosmin\u20101 signaling remain largely unknown. This protein is defective in the X\u2010linked form of Kallmann syndrome (KS) and has a prominent role in the migration of neuronal and oligodendroglial precursors. We have shown that anosmin\u20101 exerts a chemotactic effect via FGFR1 on neuronal precursors from the subventricular zone (SVZ) and the essential role of the ERK1\/2 signaling. We report here the positive chemotactic effect of FGF2 and anosmin\u20101 on rat and mouse postnatal OPCs via FGFR1. The same effect was observed with the truncated N\u2010terminal region of anosmin\u20101 (A1Nt). The introduction in anosmin\u20101 of the missense mutation F517L found in patients suffering from KS annulled the chemotactic activity; however, the mutant form carrying the disease\u2010causing mutation E514K also found in KS patients, behaved as the wild\u2010type protein. The chemoattraction exhibited by FGF2 and anosmin\u20101 on OPCs was blocked by the mitogen\u2010activated protein kinase (MAPK) inhibitor U0126, suggesting that the activation of the ERK1\/2 MAPK signaling pathway following interaction with the FGFR1 is necessary for FGF2 and anosmin\u20101 to exert their chemotactic effect. In fact, both proteins were able to induce the phosphorylation of the ERK1\/2 kinases after the activation of the FGFR1 receptor. 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