Endothelial apoptosis in Braf-deficient mice

摘要: Tyrosine kinase growth factor receptors and Ras/Raf/MEK/MAPK signalling have been implicated in the suppression1–3 as well augmentation of programmed cell death4. In addition, a Ras-independent role for Raf suppressor death has suggested by recent finding that Craf1 interacts with members Bcl-2 family at mitochondrial membranes5. However, genetic studies C elegans6 Drosophila7, targeted mutagenesis murine Araf gene8, failed to support such role. Here we show mice disruption Braf gene die vascular defects during mid-gestation. Braf−/− embryos, unlike Araf−/−8 or Craf1−/− embryos (L.W. et al., unpublished), an increased number endothelial precursor cells, dramatically enlarged blood vessels apoptotic differentiated cells. These results establish critical formation system provide first evidence essential regulation death.