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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0018270,
umls-concept:C0026609,
umls-concept:C0027834,
umls-concept:C0185117,
umls-concept:C0392756,
umls-concept:C0442038,
umls-concept:C1274040,
umls-concept:C1518284,
umls-concept:C1518286,
umls-concept:C1711351,
umls-concept:C1826396,
umls-concept:C2911684
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pubmed:issue |
6
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pubmed:dateCreated |
1995-11-6
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pubmed:abstractText |
The carboxy-terminal tail domains of neurofilament subunits neurofilament NF-M and NF-H have been postulated to be responsible for the modulation of axonal caliber. To test how subunit composition affects caliber, transgenic mice were generated to increase axonal NF-M. Total neurofilament subunit content in motor and sensory axons remained essentially unchanged, but increases in NF-M were offset by proportionate decreases in both NF-H and axonal cross-sectional area. Increase in NF-M did not affect the level of phosphorylation of NF-H. This indicates that (a) in vivo NF-H and NF-M compete either for coassembly with a limiting amount of NF-L or as substrates for axonal transport, and (b) NF-H abundance is a primary determinant of axonal caliber. Despite inhibition of radial growth, increase in NF-M and reduction in axonal NF-H did not affect nearest neighbor spacing between neurofilaments, indicating that cross-bridging between nearest neighbors does not play a crucial role in radial growth. Increase in NF-M did not result in an overt phenotype or neuronal loss, although filamentous swellings in perikarya and proximal axons of motor neurons were frequently found.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-10872323,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-1371237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-1649547,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-1718561,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-1824110,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-2120242,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-2121743,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-2586612,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-2614485,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-3138108,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-3220257,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-3312237,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-3386832,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-3472217,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-3703285,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-3843705,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-3915782,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-4176657,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-5454590,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-6166661,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-6197181,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-6425303,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-6439558,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-6540799,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-6540800,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-6577472,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-7065933,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-7230012,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-7299423,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-7519617,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-7536898,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-7721944,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-7946341,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-7965044,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-8110465,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-8376465,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-8376466,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-8446170,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-8462100,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-8462101,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-8468353,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7559762-8510825
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0021-9525
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
130
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1413-22
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7559762-Amino Acid Sequence,
pubmed-meshheading:7559762-Animals,
pubmed-meshheading:7559762-Axons,
pubmed-meshheading:7559762-Cell Communication,
pubmed-meshheading:7559762-Cell Division,
pubmed-meshheading:7559762-Intermediate Filaments,
pubmed-meshheading:7559762-Mice,
pubmed-meshheading:7559762-Mice, Transgenic,
pubmed-meshheading:7559762-Microscopy, Confocal,
pubmed-meshheading:7559762-Microscopy, Electron,
pubmed-meshheading:7559762-Molecular Sequence Data,
pubmed-meshheading:7559762-Motor Neurons
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pubmed:year |
1995
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pubmed:articleTitle |
Increasing neurofilament subunit NF-M expression reduces axonal NF-H, inhibits radial growth, and results in neurofilamentous accumulation in motor neurons.
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pubmed:affiliation |
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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