Vascular system defects and neuronal apoptosis in mice lacking Ras GTPase-activating protein

Mark Henkemeyer, Derrick J. Rossi, Douglas P. Holmyard, Mira C. Puri, Geraldine Mbamalu, Kendraprasad Harpal, T. Shane Shih, Tyler Jacks, Tony Pawson

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Abstract

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. Mutations in the Gap and Nfl 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.

Original languageEnglish (US)
Pages (from-to)695-701
Number of pages7
JournalNature
Volume377
Issue number6551
DOIs
StatePublished - Jan 1 1995

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Henkemeyer, M., Rossi, D. J., Holmyard, D. P., Puri, M. C., Mbamalu, G., Harpal, K., Shih, T. S., Jacks, T., & Pawson, T. (1995). Vascular system defects and neuronal apoptosis in mice lacking Ras GTPase-activating protein. Nature, 377(6551), 695-701. https://doi.org/10.1038/377695a0