Staying the distance: avoiding the proteasomal trap

Abstract

There are a multitude of nuclear receptor coactivators, and as a result, individual constituents of activation complexes are often overlooked when studying the specific actions of hormone signaling pathways. Specificity is typically associated with the receptor and its cognate ligand. However, SRC-3 has distinguished itself by persistent association with cell growth. In the February 29 issue of Molecular Cell, Yi et al. demonstrate that estrogen-induced posttranslational modulation of SRC-3 by atypical PKC shields it from proteasomal degradation, facilitating increased estrogenic gene activity. This process may have important implications in different types of hormone-sensitive tumors, particularly breast cancer.