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Prolactin receptor signal transduction pathways and actions determined in prolactin receptor knockout mice.

Prolactin-receptor-deficient mice are a good model in which to study the various actions of prolactin. Female homozygous knockout mice are completely infertile and show a lack of mammary development, while hemizogotes are unable to lactate following their first pregnancy. Male and female homozygotes have markedly elevated serum prolactin levels, and in some instances pituitary hyperplasia is present. Maternal behaviour is severely affected in both hemizygous and homozygous animals. Bone formation is reduced in young animals and in adults (males and females). Finally, older males and females show a slight reduction in body weight, which seems to be due to reduced abdominal fat deposition in the knockout animals.[1]

References

  1. Prolactin receptor signal transduction pathways and actions determined in prolactin receptor knockout mice. Kelly, P.A., Binart, N., Freemark, M., Lucas, B., Goffin, V., Bouchard, B. Biochem. Soc. Trans. (2001) [Pubmed]
 
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