Linked Life Data

18022325

Source:http://linkedlifedata.com/resource/pubmed/id/18022325

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-12-17
pubmed:abstractText
Mutations in the gene encoding the neural recognition molecule L1 result in hypoplasia of the corticospinal tract and path finding errors of corticospinal axons at the pyramidal decussation. Candidate molecules that have been implicated in L1-dependent guidance of corticospinal axons from the ventral medullary pyramids to the contralateral dorsal columns of the cervical spinal cord include Semaphorin3A and CD24. In the present study, we anterogradely labeled corticospinal axons from the sensorimotor cortex of young postnatal Semaphorin3A- and CD24-deficient mice to elucidate potential functions of both proteins during formation of this long axon projection. Our results indicate that elongation, collateralization, fasciculation and path finding of corticospinal axons in mice proceed normally in the absence of Semaphorin3A or CD24.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
150
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
898-904
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Development of the corticospinal tract in Semaphorin3A- and CD24-deficient mice.
pubmed:affiliation
Department of Ophthalmology, University Medical Centre Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't