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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>