Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
1997-12-10
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0969-9961
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
201-14
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Insulin-like growth factors regulate neuronal differentiation and survival.
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