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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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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.[1]

References

  1. Vascular system defects and neuronal apoptosis in mice lacking ras GTPase-activating protein. Henkemeyer, M., Rossi, D.J., Holmyard, D.P., Puri, M.C., Mbamalu, G., Harpal, K., Shih, T.S., Jacks, T., Pawson, T. Nature (1995) [Pubmed]
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