• Medientyp: E-Artikel
  • Titel: Creation and Phenotypic Analysis of α-Lactalbumin-Deficient Mice
  • Beteiligte: Stinnakre, M. G.; Vilotte, J. L.; Soulier, S.; Mercier, J. C.
  • Erschienen: National Academy of Sciences of the United States of America, 1994
  • Erschienen in: Proceedings of the National Academy of Sciences of the United States of America, 91 (1994) 14, Seite 6544-6548
  • Sprache: Englisch
  • ISSN: 0027-8424
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <p>α-Lactalbumin is an abundant milk-specific calcium metalloprotein which has an evolutionary relationship to lysozyme. It modifies the substrate specificity of a Golgi galactosyltransferase by forming the lactose synthetase binary complex. Lactose, together with other sugars and diffusible ions, is responsible for the osmotic pressure of milk. To assess the involvement of α-lactalbumin in lactogenesis, α-lactalbumin-deficient mice were created by disrupting the gene by homologous recombination in embryonic stem cells. Homozygous mutant mice are viable and fertile but females cannot feed their offspring. They produce a highly viscous milk that pups appear to be unable to remove from the mammary gland. This milk is rich in fat and protein and is devoid of α-lactalbumin and lactose. The phenotype of heterozygous mice was found to be intermediate, with a 40% decrease in α-lactalbumin but only a 10-20% decrease in the lactose content of their milk compared with wild-type animals. These results emphasize the key function of α-lactalbumin in lactogenesis and open new opportunities to manipulate milk composition.</p>
  • Zugangsstatus: Freier Zugang