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

Authors: 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 
Citation: Potenza N, etal., EMBO Rep. 2005 May;6(5):432-7.
Pubmed: (View Article at PubMed) PMID:15864294
DOI: Full-text: DOI:10.1038/sj.embor.7400397

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.

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CRRD Object Information
CRRD ID: 1581757
Created: 2006-10-24
Species: All species
Last Modified: 2006-10-24
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.