| First Author | Wojnowski L | Year | 1997 |
| Journal | Nat Genet | Volume | 16 |
| Issue | 3 | Pages | 293-7 |
| PubMed ID | 9207797 | Mgi Jnum | J:41257 |
| Mgi Id | MGI:893336 | Doi | 10.1038/ng0797-293 |
| Citation | Wojnowski L, et al. (1997) Endothelial apoptosis in Braf-deficient mice [see comments]. Nat Genet 16(3):293-7 |
| abstractText | Tyrosine kinase growth factor receptors and Ras/Raf/MEK/MAPK signalling have been implicated in the suppression as well as augmentation of programmed cell death. In addition, a Ras-independent role for Raf as a suppressor of programmed cell death has been suggested by the recent finding that Craf1 interacts with members of the Bcl-2 family at mitochondrial membranes. However, genetic studies of C. elegans and Drosophila, as well as the targeted mutagenesis of the murine Araf gene, have failed to support such a role. Here we show that mice with a targeted disruption in the Braf gene die of vascular defects during mid-gestation. Braf -/- embryos, unlike Araf -/- or Craf1 -/- embryos (L.W. et al., unpublished), show an increased number of endothelial precursor cells, dramatically enlarged blood vessels and apoptotic death of differentiated endothelial cells. These results establish Braf as a critical signalling factor in the formation of the vascular system and provide the first genetic evidence for an essential role of Raf gene in the regulation of programmed cell death. |
