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pubmed-article:9361296pubmed:abstractTextInsulin-like growth factor I (IGF-I) and IGF-II are potent trophic factors for motor and sensory neurons and glial cells. The actions of IGF-I and IGF-II are mediated via the IGF-I receptor (IGF-IR). IGF:IGF-IR binding activates distinct signaling cascades, which in turn mediate the trophic effects of the IGFs. We discuss three main IGF coupled events: growth cone motility, long-term neurite outgrowth, and neuroprotection. Our data suggest that IGF-I enhances growth cone motility by promoting reorganization of actin and activation of focal adhesion proteins via the phosphatidylinositol-3 kinase (Pl-3K) pathway. Long-term treatment with IGF-I activates the mitogen-activated protein (MAP) kinase cascade and promotes neurite outgrowth. A separable, but likely linked, action of the IGFs via Pl-3K is protection of neurons from apoptosis. These pleotrophic effects of IGFs suggest that this family of growth factors may have potential clinical utility in the treatment of neurological disorders.lld:pubmed
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pubmed-article:9361296pubmed:pagination201-14lld:pubmed
pubmed-article:9361296pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:9361296pubmed:articleTitleInsulin-like growth factors regulate neuronal differentiation and survival.lld:pubmed
pubmed-article:9361296pubmed:affiliationDepartment of Neurology, University of Michigan, Ann Arbor 48109, USA.lld:pubmed
pubmed-article:9361296pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9361296pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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