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Replacement of K-Ras with H-Ras supports normal embryonic development despite inducing cardiovascular pathology in adult mice.

Ras proteins are highly related GTPases that have key roles in regulating growth, differentiation and tumorigenesis. Gene-targeting experiments have shown that, out of the three mammalian ras genes, only K-ras is essential for normal mouse embryogenesis, and that mice deprived of H-ras and/or N-ras show no major phenotype. We generated mice (HrasKI) in which the K-ras gene had been modified to encode H-Ras protein. HrasKI mice produce undetectable amounts of K-Ras but-in contrast to mice homozygous for a null K-ras allele-they are born at the expected mendelian frequency, indicating that H-Ras can be substituted for K-Ras in embryonic development. However, adult HrasKI mice show dilated cardiomyopathy associated with arterial hypertension. Our results show that K-Ras can be replaced by H-Ras in its essential function in embryogenesis, and indicate that K-Ras has a unique role in cardiovascular homeostasis.

Pubmed ID: 15864294


  • Potenza N
  • Vecchione C
  • Notte A
  • De Rienzo A
  • Rosica A
  • Bauer L
  • Affuso A
  • De Felice M
  • Russo T
  • Poulet R
  • Cifelli G
  • De Vita G
  • Lembo G
  • Di Lauro R


EMBO reports

Publication Data

May 2, 2005

Associated Grants


Mesh Terms

  • Animals
  • Cardiomyopathy, Dilated
  • Embryonic Development
  • Genes, ras
  • Hypertension
  • Mice
  • Mice, Mutant Strains