pubmed-article:10938436 | rdf:type | pubmed:Citation | lld:pubmed |
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pubmed-article:10938436 | lifeskim:mentions | umls-concept:C1720655 | lld:lifeskim |
pubmed-article:10938436 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:10938436 | pubmed:dateCreated | 2000-10-19 | lld:pubmed |
pubmed-article:10938436 | pubmed:abstractText | The modulation of tau phosphorylation and localization in response to insulin-like growth factor-1 or insulin was examined in primary cultures of rat cortical neurons. Insulin and insulin-like growth factor-1 treatment resulted in a rapid and transient increase in tau phosphorylation at specific epitopes. These effects were completely inhibited by lithium, revealing that the insulin and insulin-like growth factor-1 induced changes in tau phosphorylation were mediated by glycogen synthase kinase-3beta. In addition, the increase in tau phosphorylation directly correlated with a transient dissociation of tau from the cytoskeleton, indicating that insulin and insulin-like growth factor-1 treatment resulted in a change in tau localization. Using immunocytochemistry, it was also demonstrated that treatment of neurons with insulin-like growth factor-1 for 3 min resulted in a redistribution of tau to the growth cone and the distal segment of the axons. Further, insulin-like growth factor-1 treatment resulted in an increased immunoreactivity with the phospho-dependent antibody AT8 in the same areas of the axons. Thus, the phosphorylation state and distribution of tau can be modulated by insulin and insulin-like growth factor-1 signaling pathways involving glycogen synthase kinase-3beta. We propose that by transiently increasing tau phosphorylation, insulin and insulin-like growth factor-1 may contribute to the reorganization of the cytoskeleton necessary for the development and growth of the neurites. | lld:pubmed |
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pubmed-article:10938436 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10938436 | pubmed:language | eng | lld:pubmed |
pubmed-article:10938436 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10938436 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:10938436 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10938436 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10938436 | pubmed:issn | 0306-4522 | lld:pubmed |
pubmed-article:10938436 | pubmed:author | pubmed-author:JohnsonG VGV | lld:pubmed |
pubmed-article:10938436 | pubmed:author | pubmed-author:LesortMM | lld:pubmed |
pubmed-article:10938436 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10938436 | pubmed:volume | 99 | lld:pubmed |
pubmed-article:10938436 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10938436 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10938436 | pubmed:pagination | 305-16 | lld:pubmed |
pubmed-article:10938436 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
pubmed-article:10938436 | pubmed:meshHeading | pubmed-meshheading:10938436... | lld:pubmed |
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pubmed-article:10938436 | pubmed:meshHeading | pubmed-meshheading:10938436... | lld:pubmed |
pubmed-article:10938436 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10938436 | pubmed:articleTitle | Insulin-like growth factor-1 and insulin mediate transient site-selective increases in tau phosphorylation in primary cortical neurons. | lld:pubmed |
pubmed-article:10938436 | pubmed:affiliation | Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Alabama 35294, USA. | lld:pubmed |
pubmed-article:10938436 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10938436 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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