SRC-3的非典型调控。

Atypical regulation of SRC-3.

作者信息

Garabedian Michael J, Logan Susan K

机构信息

Department of Microbiology, and the New York University (NYU) Cancer Institute, NYU School of Medicine, 550 First Avenue, New York, NY 10016, USA.

出版信息

Trends Biochem Sci. 2008 Jul;33(7):301-4. doi: 10.1016/j.tibs.2008.04.011. Epub 2008 May 24.

DOI:10.1016/j.tibs.2008.04.011

PMID:18502645

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.

摘要

类固醇受体辅激活因子3（SRC-3）的过表达与乳腺癌发病率增加有关。最近一项研究表明，在雌激素受体α（ERα）依赖性方式下，非典型蛋白激酶C（aPKC）介导的磷酸化可保护SRC-3免受蛋白酶体降解。这一发现为将SRC-3表达增加与雌激素依赖性细胞增殖增强联系起来提供了一种新机制。