Figure 1.

Working model of PRLrI-driven breast cancer, PRLrI expression in human breast cancer, and the PRLrI is co-transforming with the PRLrL. A, PRLrI is generated by an out-of-frame alternative splicing event, losing both the phospho-degron serine 349 (S349) as well as both putative Stat5A docking sites, tyrosines 509 and 611 (Y509 and Y611, respectively), while gaining a novel 13–amino acid tail (I-Tail). B, Altered stability and/or signaling of the PRLrL + I heterodimer, distinct from that of either homodimer, contributes to mammary transformation.