Knockout mice as model systems for studying nm23/NDP kinase gene functions. Application to the nm23-M1 gene
Related Experiment Video
Updated: Sep 23, 2026

Using Mouse Oocytes to Assess Human Gene Function During Meiosis I
Published on: April 10, 2018
S Arnaud-Dabernat1, P M Bourbon, A Dierich
1Biologie de la Différenciation et du Développement, Université Victor Segalen-Bordeaux2, Bordeaux, France.
Abstract:
Mice carrying a homozygous germ-line mutation in the nm23-M1 gene that eliminates its protein expression and drives expression of beta-galactosidase by nm23-M1 promoter have been generated. nm23-M1 gene inactivation is not teratogenic and the pups can grow to adult age without apparent health problems. However, they undergo a growth retardation and knocked out females cannot feed their pups. Both effects are background dependent. Beta-galactosidase mapping of nm23-M1 promoter activation during embryogenesis shows that the nm23-M1 gene is principally expressed in epithelial layer of tissues which require inductive epithelial-mesenchymal interactions for their formation. In conclusion, invalidated mice could be interesting models to analyze the role of nm23-M1 on signal transduction pathway regulation, or cancer induction and proliferation.
Related Concept Videos
In-vitro Mutagenesis (Gene Knockouts)
Mouse Models of Cancer Study
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...

