A necessary step toward complete functional recovery after spinal cord injury is the regeneration of axons. Axon regrowth after injury is prevented by a myriad of intrinsic and extrinsic factors. In this issue of The EMBO Journal, Huang et al () demonstrate that the cell adhesion molecule NB-3 (CNTN6) functions as a major brake on axon regrowth when it is activated by NB-3 from scar-forming cells at the injury site. Disruption of this NB-3 trans-cellular signaling led to impressive axon regrowth after spinal cord transection.
ASJC Scopus subject areas
- Molecular Biology
- Biochemistry, Genetics and Molecular Biology(all)
- Immunology and Microbiology(all)