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Cell Growth & Differentiation, Vol 7, Issue 10 1337-1344, Copyright © 1996 by American Association of Cancer Research


ARTICLES

A potential role for cell cycle control proteins in regulation of the cyclic adenosine 5'-monophosphate-responsive glycoprotein hormone alpha subunit gene

RG Pestell, C Albanese, RJ Lee, G Watanabe, E Moran, J Johnson and JL Jameson
Division of Endocrinology, Metabolism, and Molecular Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

The production of chorionic gonadotropin is coupled to the differentiation of the placenta. Expression of the alpha subunit of chorionic gonadotropin [glycoprotein hormone alpha (GPH-alpha)] is also known to be stimulated by treatment of placental cells with either cAMP or DNA synthesis inhibitors. Given these features, we used adenovirus E1A as a molecular probe to investigate a potential role for cell cycle regulatory proteins and kinases in the regulation of GPH-alpha expression. The E1A protein contains well-characterized domains that interact with a variety of cell cycle regulatory proteins. The E1A conserved regions 1 and 2 bind proteins that regulate cell cycle progression, including pRB, p107, and p130. The amino-terminal region of E1A binds several high molecular weight proteins and inhibits the transcriptional coactivator function of p300 and the homologous cAMP response element (CRE)-binding protein. We found that coexpression of E1A13S activated the GPH-alpha promoter, whereas E1A12S caused marked repression. Deletion mutants and point mutations revealed that repression by E1A12S required the CRE of the GPH-alpha promoter. Several distinct domains in E1A12S were necessary for maximal repression. A mutation of the E1A amino terminus (RG2), which inhibits binding of p300 and related high molecular weight proteins, reduced 12S repression by 40%. Mutation of the pocket protein-binding domains reduced repression by 20%, and mutations of both domains reduced repression by 80%. Overexpression of p300 or the pocket proteins (pRB, p130, and p107) induced GPH-alpha promoter activity 2-4-fold. Because the E1A amino terminus and pocket protein-binding domains together induce p34cdc2 kinase activity, the effect of p34cdc2 kinase expression on GPH-alpha activity was also assessed. Coexpression of p34cdc2 kinase or the activating p34cdc2 kinase mutant (T14AY15F) inhibited GPH-alpha promoter activity and acted through the CRE. We conclude that the GPH-alpha gene CRE is subject to regulation by cell cycle regulatory kinases and proteins.


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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1996 by the American Association of Cancer Research.