PT  - JOURNAL ARTICLE
AU  - Jinsil Park
AU  - Ben Liu
AU  - Tao Chen
AU  - Hong Li
AU  - Xuemei Hu
AU  - Jing Gao
AU  - Ying Zhu
AU  - Qiang Zhu
AU  - Boqin Qiang
AU  - Jiangang Yuan
AU  - Xiaozhong Peng
AU  - Mengsheng Qiu
TI  - Disruption of <em>Nectin-Like 1</em> Cell Adhesion Molecule Leads to Delayed Axonal Myelination in the CNS
AID  - 10.1523/JNEUROSCI.2665-08.2008
DP  - 2008 Nov 26
TA  - The Journal of Neuroscience
PG  - 12815--12819
VI  - 28
IP  - 48
4099  - http://www.jneurosci.org/content/28/48/12815.short
4100  - http://www.jneurosci.org/content/28/48/12815.full
SO  - J. Neurosci.2008 Nov 26; 28
AB  - 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.