| First Author | Arnaud-Dabernat S | Year | 2003 |
| Journal | J Bioenerg Biomembr | Volume | 35 |
| Issue | 1 | Pages | 19-30 |
| PubMed ID | 12848338 | Mgi Jnum | J:109190 |
| Mgi Id | MGI:3626054 | Doi | 10.1023/a:1023561821551 |
| Citation | Arnaud-Dabernat S, et al. (2003) Knockout mice as model systems for studying nm23/NDP kinase gene functions. Application to the nm23-M1 gene. J Bioenerg Biomembr 35(1):19-30 |
| abstractText | 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. |
