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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3-4
|
pubmed:dateCreated |
1997-12-10
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pubmed:abstractText |
Insulin-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.
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pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:issn |
0969-9961
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
4
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
201-14
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading | |
pubmed:year |
1997
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pubmed:articleTitle |
Insulin-like growth factors regulate neuronal differentiation and survival.
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pubmed:affiliation |
Department of Neurology, University of Michigan, Ann Arbor 48109, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, Non-U.S. Gov't
|