Prolactin signaling and Stat5: going their own separate ways?
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* Corresponding author: Cathrin Brisken Cathrin.Brisken@isrec.unil.ch
1 Swiss Institute for Experimental Cancer Research, Epalinges, Switzerland
2 University of Innsbruck, Medical Chemistry and Biochemistry, Innsbruck, Austria
Breast Cancer Res 2002, 4:209-212 doi:10.1186/bcr543
Published: 3 October 2002Abstract
Miyoshi et al. compared the role of the prolactin receptor (PrlR) and its downstream mediator, the signal transducer and activator of transcription 5 (Stat5), in mammary epithelial cells in vivo by studying PrlR-/- and Stat5ab-/- mouse mammary epithelial transplants during pregnancy. At first glance, the two mutant epithelia appear to have similar defects in the differentiation of the alveolar epithelium. However, a closer examination by Miyoshi et al. revealed defects in the epithelial architecture of the smallest ducts of Stat5ab-/- transplants not apparent in the PrlR-/- transplants, suggesting that Stat5 is more than a simple mediator of PrlR action.