Knockout Mice as Model Systems for Studying nm23/NDP Kinase Gene Functions. Application to the nm23-M1 Gene

J Bioenerg Biomembr. 2003 Feb;35(1):19-30. doi: 10.1023/a:1023561821551.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • 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

Substances

  • NM23 Nucleoside Diphosphate Kinases
  • Proteins
  • Recombinant Proteins
  • Nme1 protein, mouse
  • Nucleoside-Diphosphate Kinase