| pubmed-article:18687773 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18687773 | lifeskim:mentions | umls-concept:C0229992 | lld:lifeskim |
| pubmed-article:18687773 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
| pubmed-article:18687773 | lifeskim:mentions | umls-concept:C1160340 | lld:lifeskim |
| pubmed-article:18687773 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:18687773 | pubmed:dateCreated | 2008-11-21 | lld:pubmed |
| pubmed-article:18687773 | pubmed:abstractText | Signaling through the type 1 IGF receptor (IGF1R) after interaction with IGF-I is crucial to the normal brain development. Manipulations of the mouse genome leading to changes in the expression of IGF-I or IGF1R significantly alters brain growth, such that IGF-I overexpression leads to brain overgrowth, whereas null mutations in either IGF-I or the IGF1R result in brain growth retardation. IGF-I signaling stimulates the proliferation, survival, and differentiation of each of the major neural lineages, neurons, oligodendrocytes, and astrocytes, as well as possibly influencing neural stem cells. During embryonic life, IGF-I stimulates neuron progenitor proliferation, whereas later it promotes neuron survival, neuritic outgrowth, and synaptogenesis. IGF-I also stimulates oligodendrocyte progenitor proliferation although inhibiting apoptosis in oligodendrocyte lineage cells and stimulating myelin production. These pleiotropic IGF-I activities indicate that other factors provide instructive signals for specific cellular events and that IGF-I acts to facilitate them. Studies of the few humans with IGF-I and/or IGF1R gene mutations indicate that IGF-I serves a similar role in man. | lld:pubmed |
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| pubmed-article:18687773 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18687773 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:18687773 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18687773 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:18687773 | pubmed:issn | 0013-7227 | lld:pubmed |
| pubmed-article:18687773 | pubmed:author | pubmed-author:YePingP | lld:pubmed |
| pubmed-article:18687773 | pubmed:author | pubmed-author:Joseph... | lld:pubmed |
| pubmed-article:18687773 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18687773 | pubmed:volume | 149 | lld:pubmed |
| pubmed-article:18687773 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18687773 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18687773 | pubmed:pagination | 5958-62 | lld:pubmed |
| pubmed-article:18687773 | pubmed:dateRevised | 2010-9-21 | lld:pubmed |
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| pubmed-article:18687773 | pubmed:meshHeading | pubmed-meshheading:18687773... | lld:pubmed |
| pubmed-article:18687773 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18687773 | pubmed:articleTitle | Expanding the mind: insulin-like growth factor I and brain development. | lld:pubmed |
| pubmed-article:18687773 | pubmed:affiliation | Department of Pediatrics, CB 7039, University of North Carolina, Chapel Hill, North Carolina 27599-7039, USA. ajd@med.unc.edu | lld:pubmed |
| pubmed-article:18687773 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18687773 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:18687773 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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