Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1997-4-22
pubmed:abstractText
beta-Tubulin is encoded by a family of genes that produces at least five distinct polypeptide isotypes in neurons. Two of these isotypes (i.e., classes II and III) preferentially accumulate in axons, and the expression of one of them (i.e., class II) correlates closely with axonal outgrowth during development and regeneration. In dorsal root ganglion (DRG) neurons, expression of the class II isotype declines to relatively low levels during early postnatal development, and increases dramatically in mature neurons during axon regeneration (i.e., to a level comparable to that in developing neurons). In contrast, expression of the class III isotype, which rises slightly during postnatal development, increases much less than the class II isotype during regeneration. We now document that these changes in gene expression are associated with an increase in the relative amount of class II as compared to class III beta-tubulin delivered to regenerating sensory axons of rat sciatic nerve by slow axonal transport. In this study, the tubulin transported in sensory axons was labeled by injecting [35S]methionine into the L5 DRG either 7 or 14 days after crushing the sciatic nerve; pulse-labeled class II and class III beta-tubulin were identified using immunoprecipitation. This change in the isotype composition of beta-tubulin transported in regenerating axons may influence outgrowth by altering the assembly and dynamic properties of axonal microtubules.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
742
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
329-33
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Changes in the isotype composition of beta-tubulin delivered to regenerating sensory axons by slow axonal transport.
pubmed:affiliation
Department of Ophthalmology, The Johns Hopkins School of Medicine, Baltimore, MD 21287-6953, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't