PMID:12848338

Citation	Arnaud-Dabernat, S, Bourbon, PM, Dierich, A, Le Meur, M and Daniel, JY (2003) Knockout mice as model systems for studying nm23/NDP kinase gene functions. Application to the nm23-M1 gene. J. Bioenerg. Biomembr. 35:19-30
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.
Links	PubMed
Keywords	Animals; Animals, Newborn; Breast/metabolism; Cloning, Molecular; Female; Fetal Growth Retardation/genetics; Fetal Growth Retardation/metabolism; Gene Expression Regulation, Developmental/genetics; Gene Expression Regulation, Enzymologic/genetics; Mice; Mice, Knockout/embryology; Mice, Knockout/growth & development; Mice, Knockout/metabolism; Models, Animal; NM23 Nucleoside Diphosphate Kinases; Nucleoside-Diphosphate Kinase; Proteins/genetics; Proteins/metabolism; Recombinant Proteins/genetics; Recombinant Proteins/metabolism; Signal Transduction/genetics; Structure-Activity Relationship
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.