Files in this item



application/pdf3269858.pdf (2MB)Restricted to U of Illinois
(no description provided)PDF


Title:Studies of Estrogen Receptor's Roles in Tamoxifen-Induced Apoptosis and the Regulation of Gene Expression
Author(s):Cheng, Jingwei
Doctoral Committee Chair(s):Shapiro, David J.
Department / Program:Biochemistry
Degree Granting Institution:University of Illinois at Urbana-Champaign
Subject(s):Biology, Molecular
Abstract:Parallel work done by my colleague suggests that long-term activation of the ERK1/2 signal transduction pathway also plays an important role in OHT-induced apoptosis. To understand the connection between ERK1/2 activation and ER mediated gene expression, I chose serine 118 of ERalpha for further study. Serine 118 is a critical MAPK kinase phosphorylation site in ERalpha. To avoid potential artifacts due to transient transfection and use of artificial estrogen response element (ERE)-containing reporter genes, I isolated stably transfected cell lines that express the ERalphaS118A phosphorylation site mutant. Using stably transfected HeLa cell lines with functional ERK1/2 activity and expressing similar levels of wild-type ERalpha and ERalphaS118A, I compared expression of several classes of endogenous estrogen and tamoxifen-regulated genes. I concluded that phosphorylation of serine 118 is important for ER mediated gene transcription on some ERE-containing cellular genes while playing little role on other genes. Although estrogen and tamoxifen down-regulate numerous genes, mechanisms remain poorly understood. Interestingly, my data suggests a previously unknown requirement for serine 118 phosphorylation in estrogen and tamoxifen mediated gene down-regulation of gene expression.
Issue Date:2007
Description:112 p.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2007.
Other Identifier(s):(MiAaPQ)AAI3269858
Date Available in IDEALS:2015-09-25
Date Deposited:2007

This item appears in the following Collection(s)

Item Statistics