| First Author | Camarero G | Year | 2006 |
| Journal | Mol Cell Biol | Volume | 26 |
| Issue | 19 | Pages | 7103-15 |
| PubMed ID | 16980614 | Mgi Jnum | J:112971 |
| Mgi Id | MGI:3664149 | Doi | 10.1128/MCB.00424-06 |
| Citation | Camarero G, et al. (2006) Cortical migration defects in mice expressing A-RAF from the B-RAF locus. Mol Cell Biol 26(19):7103-15 |
| abstractText | We have previously shown that mice lacking the protein kinase B-RAF have defects in both neural and endothelial cell lineages and die around embryonic day 12 (E12). To delineate the function of B-RAF in the brain, B-RAF KIN/KIN mice lacking B-RAF and expressing A-RAF under the control of the B-RAF locus were created. B-RAF KIN/KIN embryos displayed no vascular defects, no endothelial and neuronal apoptosis, or gross developmental abnormalities, and a significant proportion of these animals survived for up to 8 weeks. Cell proliferation in the neocortex was reduced from E14.5 onwards. Newborn cortical neurons were impaired in their migration toward the cortical plate, causing a depletion of Brn-2-expressing pyramidal neurons in layers II, III, and V of the postnatal cortex. Our data reveal that B-RAF is an important mediator of neuronal survival, migration, and dendrite formation and that A-RAF cannot fully compensate for these functions. |
