Vascular system defects and neuronal apoptosis in mice lacking ras GTPase-activating protein.
The gene encoding p120-rasGAP, a negative regulator of Ras, has been disrupted in mice. This Gap mutation affects the ability of endothelial cells to organize into a highly vascularized network and results in extensive neuronal cell death. Mutati ons in the Gap and Nf1 genes have a synergistic effect, such that embryos homozygous for mutations in both genes show an exacerbated Gap phenotype. Thus rasGAP and neurofibromin act together to regulate Ras activity during embryonic development.
D000818:Animals; D001483:Base Sequence; D002319:Cardiovascular System / Q000196:embryology*; D016923:Cell Death / Q000235:genetics; D002460:Cell Line; D002678:Chimera; D005314:Embryonic and Fetal Development / Q000235:genetics / Q000502:physiology*; D005260:Female; D005313:Fetal Death / Q000235:genetics; D020558:GTP Phosphohydrolases; D020690:GTPase-Activating Proteins; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008969:Molecular Sequence Data; D016296:Mutagenesis; D025542:Neurofibromin 1; D011506:Proteins / Q000235:genetics / Q000502:physiology*; D020703:ras GTPase-Activating Proteins; D018631:ras Proteins / Q000502:physiology
D020690:GTPase-Activating Proteins; D025542:Neurofibromin 1; D011506:Proteins; D020703:ras GTPase-Activating Proteins; D020558:GTP Phosphohydrolases; D018631:ras Proteins