pubmed-article:10084688 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10084688 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:10084688 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
pubmed-article:10084688 | lifeskim:mentions | umls-concept:C0282587 | lld:lifeskim |
pubmed-article:10084688 | lifeskim:mentions | umls-concept:C0521390 | lld:lifeskim |
pubmed-article:10084688 | lifeskim:mentions | umls-concept:C0056695 | lld:lifeskim |
pubmed-article:10084688 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:10084688 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:10084688 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:10084688 | pubmed:dateCreated | 1999-5-11 | lld:pubmed |
pubmed-article:10084688 | pubmed:abstractText | The neural cell adhesion molecule NCAM plays an important role in axonal growth, learning, and memory. A signaling pathway has been elucidated in which clustering of the NCAM140 isoform in the neural plasma membrane stimulated the activating phosphorylation of mitogen-activated protein kinases (MAPKs) and the transcription factor cyclic AMP response-element binding protein (CREB). NCAM clustering transiently induced dual phosphorylation (activation) of the MAPKs ERK1 and ERK2 (extracellular signal-regulated kinases) by a pathway regulated by the focal adhesion kinase p125fak, p59fyn, Ras, and MAPK kinase. CREB phosphorylation at serine 133 induced by NCAM was dependent in part on an intact MAPK pathway. c-Jun N-terminal kinase, which is associated with apoptosis and cellular stress, was not activated by NCAM. Inhibition of the MAPK pathway in rat cerebellar neuron cultures selectively reduced NCAM-stimulated neurite outgrowth. These results define an NCAM signal transduction mechanism with the potential for modulating the expression of genes needed for axonal growth, survival, and synaptic plasticity. | lld:pubmed |
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pubmed-article:10084688 | pubmed:language | eng | lld:pubmed |
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pubmed-article:10084688 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:10084688 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10084688 | pubmed:month | Mar | lld:pubmed |
pubmed-article:10084688 | pubmed:issn | 0022-3034 | lld:pubmed |
pubmed-article:10084688 | pubmed:author | pubmed-author:ChenSS | lld:pubmed |
pubmed-article:10084688 | pubmed:author | pubmed-author:SchachnerMM | lld:pubmed |
pubmed-article:10084688 | pubmed:author | pubmed-author:ManessP FPF | lld:pubmed |
pubmed-article:10084688 | pubmed:author | pubmed-author:SchallerM DMD | lld:pubmed |
pubmed-article:10084688 | pubmed:author | pubmed-author:HemperlyJ JJJ | lld:pubmed |
pubmed-article:10084688 | pubmed:author | pubmed-author:SchildR JRJ | lld:pubmed |
pubmed-article:10084688 | pubmed:author | pubmed-author:GraffR DRD | lld:pubmed |
pubmed-article:10084688 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10084688 | pubmed:volume | 38 | lld:pubmed |
pubmed-article:10084688 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10084688 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10084688 | pubmed:pagination | 542-58 | lld:pubmed |
pubmed-article:10084688 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:10084688 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10084688 | pubmed:articleTitle | NCAM stimulates the Ras-MAPK pathway and CREB phosphorylation in neuronal cells. | lld:pubmed |
pubmed-article:10084688 | pubmed:affiliation | Department of Biochemistry, School of Medicine, University of North Carolina, Chapel Hill 27599-7260, USA. | lld:pubmed |
pubmed-article:10084688 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10084688 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:10084688 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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