| First Author | Park J | Year | 2008 |
| Journal | J Neurosci | Volume | 28 |
| Issue | 48 | Pages | 12815-9 |
| PubMed ID | 19036974 | Mgi Jnum | J:142504 |
| Mgi Id | MGI:3821638 | Doi | 10.1523/JNEUROSCI.2665-08.2008 |
| Citation | Park J, et al. (2008) Disruption of Nectin-like 1 cell adhesion molecule leads to delayed axonal myelination in the CNS. J Neurosci 28(48):12815-9 |
| abstractText | Nectin-like 1 (Necl-1) is a neural-specific cell adhesion molecule that is expressed in both the CNS and PNS. Previous in vitro studies suggested that Necl-1 expression is essential for the axon-glial interaction and myelin sheath formation in the PNS. To investigate the in vivo role of Necl-1 in axonal myelination of the developing nervous system, we generated the Necl-1 mutant mice by replacing axons 2-5 with the LacZ reporter gene. Expression studies revealed that Necl-1 is exclusively expressed by neurons in the CNS. Disruption of Necl-1 resulted in developmental delay of axonal myelination in the optic nerve and spinal cord, suggesting that Necl-1 plays an important role in the initial axon-oligodendrocyte recognition and adhesion in CNS myelination. |
