Studies of Estrogen Receptor's Roles in Tamoxifen-Induced Apoptosis and the Regulation of Gene Expression
Cheng, Jingwei
This item is only available for download by members of the University of Illinois community. Students, faculty, and staff at the U of I may log in with your NetID and password to view the item. If you are trying to access an Illinois-restricted dissertation or thesis, you can request a copy through your library's Inter-Library Loan office or purchase a copy directly from ProQuest.
Permalink
https://hdl.handle.net/2142/84839
Description
Title
Studies of Estrogen Receptor's Roles in Tamoxifen-Induced Apoptosis and the Regulation of Gene Expression
Author(s)
Cheng, Jingwei
Issue Date
2007
Doctoral Committee Chair(s)
Shapiro, David J.
Department of Study
Biochemistry
Discipline
Biochemistry
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Molecular
Language
eng
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.
Use this login method if you
don't
have an
@illinois.edu
email address.
(Oops, I do have one)
IDEALS migrated to a new platform on June 23, 2022. If you created
your account prior to this date, you will have to reset your password
using the forgot-password link below.
