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Atypical regulation of SRC-3
Authors:Garabedian Michael J  Logan Susan K
Affiliation:Department of Microbiology, and the New York University (NYU) Cancer Institute, NYU School of Medicine, 550 First Avenue, New York, NY 10016, USA. michael.garabedian@nyumc.org
Abstract:Overexpression of steroid receptor coactivator 3 (SRC-3) is associated with an increased incidence of breast cancer. A recent study shows that SRC-3 is protected from proteasomal degradation by atypical protein kinase C (aPKC)-mediated phosphorylation in an estrogen receptor alpha (ERalpha)-dependent manner. This finding provides a novel mechanism for coupling increased SRC-3 expression with enhanced estrogen-dependent cellular proliferation.
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