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Publication : Development of the corticospinal tract in Semaphorin3A- and CD24-deficient mice.

First Author  Sibbe M Year  2007
Journal  Neuroscience Volume  150
Issue  4 Pages  898-904
PubMed ID  18022325 Mgi Jnum  J:130761
Mgi Id  MGI:3772299 Doi  10.1016/j.neuroscience.2007.10.007
Citation  Sibbe M, et al. (2007) Development of the corticospinal tract in Semaphorin3A- and CD24-deficient mice. Neuroscience 150(4):898-904
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.
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