The Akt pathway plays a central role in regulating cell survival, proliferation and metabolism and is one of the most commonly activated pathways in human cancer. A role for Akt in epithelial differentiation, however, has not been established. We previously reported that mice lacking Akt1, but not Akt2, exhibit a pronounced metabolic defect during late pregnancy and lactation that results from a failure to up-regulate glucose transporter 1 (Glut1) as well as several lipid synthetic enzymes. Despite this metabolic defect, however, both Akt1-deficient and Akt2-deficient mice exhibit normal mammary epithelial differentiation and signal transducer and activator of transcription 5 (Stat5) activation.
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09/17/10