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Publication : Creation and phenotypic analysis of alpha-lactalbumin-deficient mice.

First Author  Stinnakre MG Year  1994
Journal  Proc Natl Acad Sci U S A Volume  91
Issue  14 Pages  6544-8
PubMed ID  8022817 Mgi Jnum  J:19377
Mgi Id  MGI:67543 Doi  10.1073/pnas.91.14.6544
Citation  Stinnakre MG, et al. (1994) Creation and phenotypic analysis of alpha-lactalbumin-deficient mice. Proc Natl Acad Sci U S A 91(14):6544-8
abstractText  alpha-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 alpha-lactalbumin in lactogenesis, alpha-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 alpha-lactalbumin and lactose. The phenotype of heterozygous mice was found to be intermediate, with a 40% decrease in alpha-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 alpha-lactalbumin in lactogenesis and open new opportunities to manipulate milk composition.
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