| pubmed-article:10423273 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10423273 | lifeskim:mentions | umls-concept:C0027834 | lld:lifeskim |
| pubmed-article:10423273 | lifeskim:mentions | umls-concept:C0085103 | lld:lifeskim |
| pubmed-article:10423273 | lifeskim:mentions | umls-concept:C0815000 | lld:lifeskim |
| pubmed-article:10423273 | lifeskim:mentions | umls-concept:C0021769 | lld:lifeskim |
| pubmed-article:10423273 | lifeskim:mentions | umls-concept:C0081527 | lld:lifeskim |
| pubmed-article:10423273 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:10423273 | pubmed:dateCreated | 1999-10-14 | lld:pubmed |
| pubmed-article:10423273 | pubmed:abstractText | We examined the localization and role of alpha-IN vs. other neuronal intermediate filaments before and during differentiation. Vimentin but not alpha-IN localized within filopodia-like neurites of undifferentiated cells. During differentiation, alpha-IN immunoreactivity accumulated within axonal neurites following vimentin but, as previously describe in neurons in situ, before the appearance of NF-L. We therefore manipulated alpha-IN synthesis, accumulation, and function in attempts to determine whether or not this intermediate filament species played a role in axonal development. Intracellular delivery of anti-alpha-IN antisense oligonucleotides and antibodies was permissive for neuritogenesis, yet compromised neurite elongation; this effect was further reflected in diminished levels of stabilized axonal microtubules. These data suggest that alpha-IN plays a role in the development of neuronal polarity. Relatively more alpha-IN than NF-L accumulated within the plastic axonal neurites induced following serum-deprivation, while stable, dbcAMP-induced neurites treatment contained equivalent levels of each. Protease inhibition increased NF-L and NF-H but not alpha-IN immunoreactivity within serum-deprived neurites, suggesting that proteolysis restricts NF-L accumulation pending neurite stabilization. To test the possibility that NF-H accumulation is dependent upon NF-L and cannot be mediated by alpha-IN, we examined levels of NF-H co-precipitated from cells with alpha-IN and NF-L. Virtually all newly synthesized NF-H co-precipitated with NF-L, while only a small percentage co-precipitated with alpha-IN. Finally, NF-H or NF-M were absent from the axon hillock or perikaryal area at the base of neurites, where alpha-IN immunoreactivity is prominent. These data extend earlier cell-free demonstrations that NF-H preferentially associates with NF-L rather than alpha-IN. | lld:pubmed |
| pubmed-article:10423273 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10423273 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10423273 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10423273 | pubmed:issn | 0886-1544 | lld:pubmed |
| pubmed-article:10423273 | pubmed:author | pubmed-author:SheaT BTB | lld:pubmed |
| pubmed-article:10423273 | pubmed:author | pubmed-author:BeermannM LML | lld:pubmed |
| pubmed-article:10423273 | pubmed:copyrightInfo | Copyright 1999 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:10423273 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10423273 | pubmed:volume | 43 | lld:pubmed |
| pubmed-article:10423273 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10423273 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10423273 | pubmed:pagination | 322-33 | lld:pubmed |
| pubmed-article:10423273 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:10423273 | pubmed:meshHeading | pubmed-meshheading:10423273... | lld:pubmed |
| pubmed-article:10423273 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10423273 | pubmed:articleTitle | Neuronal intermediate filament protein alpha-internexin facilitates axonal neurite elongation in neuroblastoma cells. | lld:pubmed |
| pubmed-article:10423273 | pubmed:affiliation | Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts at Lowell, Lowell 01854, USA. Thomas_Shea@uml.edu | lld:pubmed |
| pubmed-article:10423273 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10423273 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10423273 | lld:pubmed |
