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It has now been over 60 years since Riddle et al. (1) purified a hormone from the anterior pituitary gland, which stimulated milk secretion in the mammary gland of virgin rabbits. They named it prolactin (PRL).1 Since then, the synergistic approaches of biochemistry, physiology, molecular biology, and cell biology have unveiled several molecular switches in the PRL signaling cascade (Fig. 1). Loss-of-function studies in the mouse have now provided clear insight into the biology of two components of the PRL pathway.
Hennighausen et al. (Sat,) studied this question.
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