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

Nature. 1995 Oct 26;377(6551):695-701. doi: 10.1038/377695a0.

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. 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cardiovascular System / embryology*
  • Cell Death / genetics
  • Cell Line
  • Chimera
  • Embryonic and Fetal Development / genetics
  • Embryonic and Fetal Development / physiology*
  • Female
  • Fetal Death / genetics
  • GTP Phosphohydrolases*
  • GTPase-Activating Proteins
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Molecular Sequence Data
  • Mutagenesis
  • Neurofibromin 1
  • Proteins / genetics
  • Proteins / physiology*
  • ras GTPase-Activating Proteins
  • ras Proteins* / physiology

Substances

  • GTPase-Activating Proteins
  • Neurofibromin 1
  • Proteins
  • ras GTPase-Activating Proteins
  • GTP Phosphohydrolases
  • ras Proteins