| First Author | Hajj GN | Year | 2007 |
| Journal | J Cell Sci | Volume | 120 |
| Issue | Pt 11 | Pages | 1915-26 |
| PubMed ID | 17504807 | Mgi Jnum | J:124048 |
| Mgi Id | MGI:3720434 | Doi | 10.1242/jcs.03459 |
| Citation | Hajj GN, et al. (2007) Cellular prion protein interaction with vitronectin supports axonal growth and is compensated by integrins. J Cell Sci 120(Pt 11):1915-26 |
| abstractText | The physiological functions of the cellular prion protein, PrP(C), as a cell surface pleiotropic receptor are under debate. We report that PrP(C) interacts with vitronectin but not with fibronectin or collagen. The binding sites mediating this PrP(C)-vitronectin interaction were mapped to residues 105-119 of PrP(C) and the residues 307-320 of vitronectin. The two proteins were co-localized in embryonic dorsal root ganglia from wild-type mice. Vitronectin addition to cultured dorsal root ganglia induced axonal growth, which could be mimicked by vitronectin peptide 307-320 and abrogated by anti-PrP(C) antibodies. Full-length vitronectin, but not the vitronectin peptide 307-320, induced axonal growth of dorsal root neurons from two strains of PrP(C)-null mice. Functional assays demonstrated that relative to wild-type cells, PrP(C)-null dorsal root neurons were more responsive to the Arg-Gly-Asp peptide (an integrin-binding site), and exhibited greater alphavbeta3 activity. Our findings indicate that PrP(C) plays an important role in axonal growth, and this function may be rescued in PrP(C)-knockout animals by integrin compensatory mechanisms. |
